The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonized particles, immune complexes, and chemotactic factors, bind to specific cell-surface receptors on the neutrophil.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
A formylated tripeptide originally isolated from bacterial filtrates that is positively chemotactic to polymorphonuclear leucocytes, and causes them to release lysosomal enzymes and become metabolically activated.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.
A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (GRANULOMATOUS DISEASE, CHRONIC) often die as a result of recurrent bacterial infections.
An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.
A CD antigen that contains a conserved I domain which is involved in ligand binding. When combined with CD18 the two subunits form MACROPHAGE-1 ANTIGEN.
The process of losing secretory granules (SECRETORY VESICLES). This occurs, for example, in mast cells, basophils, neutrophils, eosinophils, and platelets when secretory products are released from the granules by EXOCYTOSIS.
A polymorphonuclear leukocyte-derived serine protease that degrades proteins such as ELASTIN; FIBRONECTIN; LAMININ; VITRONECTIN; and COLLAGEN. It is named for its ability to control myeloid cell growth and differentiation.
Cell adhesion molecule and CD antigen that serves as a homing receptor for lymphocytes to lymph node high endothelial venules.
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
A protease of broad specificity, obtained from dried pancreas. Molecular weight is approximately 25,000. The enzyme breaks down elastin, the specific protein of elastic fibers, and digests other proteins such as fibrin, hemoglobin, and albumin. EC 3.4.21.36.
Autoantibodies directed against cytoplasmic constituents of POLYMORPHONUCLEAR LEUKOCYTES and/or MONOCYTES. They are used as specific markers for GRANULOMATOSIS WITH POLYANGIITIS and other diseases, though their pathophysiological role is not clear. ANCA are routinely detected by indirect immunofluorescence with three different patterns: c-ANCA (cytoplasmic), p-ANCA (perinuclear), and atypical ANCA.
Chemical substances that attract or repel cells. The concept denotes especially those factors released as a result of tissue injury, microbial invasion, or immunologic activity, that attract LEUKOCYTES; MACROPHAGES; or other cells to the site of infection or insult.
The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.
An enzyme that catalyzes the hydrolysis of proteins, including elastin. It cleaves preferentially bonds at the carboxyl side of Ala and Val, with greater specificity for Ala. EC 3.4.21.37.
A condition occurring as a result of exposure to a rapid fall in ambient pressure. Gases, nitrogen in particular, come out of solution and form bubbles in body fluid and blood. These gas bubbles accumulate in joint spaces and the peripheral circulation impairing tissue oxygenation causing disorientation, severe pain, and potentially death.
Adherence of cells to surfaces or to other cells.
A family of G-protein-coupled receptors that was originally identified by its ability to bind N-formyl peptides such as N-FORMYLMETHIONINE LEUCYL-PHENYLALANINE. Since N-formyl peptides are found in MITOCHONDRIA and BACTERIA, this class of receptors is believed to play a role in mediating cellular responses to cellular damage and bacterial invasion. However, non-formylated peptide ligands have also been found for this receptor class.
Techniques used for determining the values of photometric parameters of light resulting from LUMINESCENCE.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990)
An iron-binding protein that was originally characterized as a milk protein. It is widely distributed in secretory fluids and is found in the neutrophilic granules of LEUKOCYTES. The N-terminal part of lactoferrin possesses a serine protease which functions to inactivate the TYPE III SECRETION SYSTEM used by bacteria to export virulence proteins for host cell invasion.
A CXC chemokine with specificity for CXCR2 RECEPTORS. It has growth factor activities and is implicated as a oncogenic factor in several tumor types.
High-affinity G-protein-coupled receptors for INTERLEUKIN-8 present on NEUTROPHILS; MONOCYTES; and BASOPHILS.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
Zymosan is a polysaccharide derived from the cell walls of Saccharomyces cerevisiae, commonly used in research as an immunostimulant to induce inflammation and study phagocytosis, complement activation, and oxidative burst in neutrophils and macrophages.
Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
The number of WHITE BLOOD CELLS per unit volume in venous BLOOD. A differential leukocyte count measures the relative numbers of the different types of white cells.
A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, pre-eclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders.
An inorganic pyrophosphate which affects calcium metabolism in mammals. Abnormalities in its metabolism occur in some human diseases, notably HYPOPHOSPHATASIA and pseudogout (CHONDROCALCINOSIS).
A cytotoxic member of the CYTOCHALASINS.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
High-affinity G-protein-coupled receptors for INTERLEUKIN-8 present on NEUTROPHILS; MONOCYTES; and T-LYMPHOCYTES. These receptors also bind several other CXC CHEMOKINES.
Condensed areas of cellular material that may be bounded by a membrane.
A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.
A flavoprotein enzyme that catalyzes the univalent reduction of OXYGEN using NADPH as an electron donor to create SUPEROXIDE ANION. The enzyme is dependent on a variety of CYTOCHROMES. Defects in the production of superoxide ions by enzymes such as NADPH oxidase result in GRANULOMATOUS DISEASE, CHRONIC.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Extracellular vesicles generated by the shedding of CELL MEMBRANE blebs.
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Shock produced as a result of trauma.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent DECOMPRESSION SICKNESS. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings.
A group of three different alpha chains (CD11a, CD11b, CD11c) that are associated with an invariant CD18 beta chain (ANTIGENS, CD18). The three resulting leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE ADHESION) are LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; MACROPHAGE-1 ANTIGEN; and ANTIGEN, P150,95.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Transmembrane proteins consisting of a lectin-like domain, an epidermal growth factor-like domain, and a variable number of domains that are homologous to complement regulatory proteins. They are important cell adhesion molecules which help LEUKOCYTES attach to VASCULAR ENDOTHELIUM.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A multisystemic disease of a complex genetic background. It is characterized by inflammation of the blood vessels (VASCULITIS) leading to damage in any number of organs. The common features include granulomatous inflammation of the RESPIRATORY TRACT and kidneys. Most patients have measurable autoantibodies (ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES) against neutrophil proteinase-3 (WEGENER AUTOANTIGEN).
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.
A subclass of lipid-linked proteins that contain a GLYCOSYLPHOSPHATIDYLINOSITOL LINKAGE which holds them to the CELL MEMBRANE.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
A 10.8-kDa member of the S-100 family of calcium-binding proteins that can form homo- or heterocomplexes with CALGRANULIN B and a variety of other proteins. The calgranulin A/B heterodimer is known as LEUKOCYTE L1 ANTIGEN COMPLEX. Calgranulin A is found in many cell types including GRANULOCYTES; KERATINOCYTES; and myelomonocytes, and has been shown to act as a chemotactic substance for NEUTROPHILS. Because it is present in acute inflammation but absent in chronic inflammation, it is a useful biological marker for a number of pathological conditions.
An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
Washing liquid obtained from irrigation of the lung, including the BRONCHI and the PULMONARY ALVEOLI. It is generally used to assess biochemical, inflammatory, or infection status of the lung.
The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A condition of lung damage that is characterized by bilateral pulmonary infiltrates (PULMONARY EDEMA) rich in NEUTROPHILS, and in the absence of clinical HEART FAILURE. This can represent a spectrum of pulmonary lesions, endothelial and epithelial, due to numerous factors (physical, chemical, or biological).
An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages.
A group of oxidoreductases that act on NADH or NADPH. In general, enzymes using NADH or NADPH to reduce a substrate are classified according to the reverse reaction, in which NAD+ or NADP+ is formally regarded as an acceptor. This subclass includes only those enzymes in which some other redox carrier is the acceptor. (Enzyme Nomenclature, 1992, p100) EC 1.6.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
Acute hemorrhage or excessive fluid loss resulting in HYPOVOLEMIA.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.
The phenomenon by which dissociated cells intermixed in vitro tend to group themselves with cells of their own type.
Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.
Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C; (CHEMOKINES, C); CC; (CHEMOKINES, CC); and CXC; (CHEMOKINES, CXC); according to variations in a shared cysteine motif.
Elements of limited time intervals, contributing to particular results or situations.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.
Group of chemokines with paired cysteines separated by a different amino acid. CXC chemokines are chemoattractants for neutrophils but not monocytes.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Antibodies produced by a single clone of cells.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
Glycoproteins found on the membrane or surface of cells.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Substances that reduce or suppress INFLAMMATION.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.
Inbred BALB/c mice are a strain of laboratory mice that have been selectively bred to be genetically identical to each other, making them useful for scientific research and experiments due to their consistent genetic background and predictable responses to various stimuli or treatments.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
An activity in which the organism plunges into water. It includes scuba and bell diving. Diving as natural behavior of animals goes here, as well as diving in decompression experiments with humans or animals.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
A condition characterized by the presence of ENDOTOXINS in the blood. On lysis, the outer cell wall of gram-negative bacteria enters the systemic circulation and initiates a pathophysiologic cascade of pro-inflammatory mediators.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
A serine protease found in the azurophil granules of NEUTROPHILS. It has an enzyme specificity similar to that of chymotrypsin C.
Proteins prepared by recombinant DNA technology.
Glucuronidase is an enzyme (specifically, a glycosidase) that catalyzes the hydrolysis of glucuronic acid from various substrates, playing crucial roles in metabolic processes like detoxification and biotransformation within organisms.
The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).
Infection of the lung often accompanied by inflammation.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The rate dynamics in chemical or physical systems.
A pattern recognition receptor that interacts with LYMPHOCYTE ANTIGEN 96 and LIPOPOLYSACCHARIDES. It mediates cellular responses to GRAM-NEGATIVE BACTERIA.
A set of BACTERIAL ADHESINS and TOXINS, BIOLOGICAL produced by BORDETELLA organisms that determine the pathogenesis of BORDETELLA INFECTIONS, such as WHOOPING COUGH. They include filamentous hemagglutinin; FIMBRIAE PROTEINS; pertactin; PERTUSSIS TOXIN; ADENYLATE CYCLASE TOXIN; dermonecrotic toxin; tracheal cytotoxin; Bordetella LIPOPOLYSACCHARIDES; and tracheal colonization factor.
Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
A basic enzyme that is present in saliva, tears, egg white, and many animal fluids. It functions as an antibacterial agent. The enzyme catalyzes the hydrolysis of 1,4-beta-linkages between N-acetylmuramic acid and N-acetyl-D-glucosamine residues in peptidoglycan and between N-acetyl-D-glucosamine residues in chitodextrin. EC 3.2.1.17.
One of the virulence factors produced by BORDETELLA PERTUSSIS. It is a multimeric protein composed of five subunits S1 - S5. S1 contains mono ADPribose transferase activity.
A CXC chemokine that is synthesized by activated MONOCYTES and NEUTROPHILS. It has specificity for CXCR2 RECEPTORS.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. When chronic granulomatous disease is caused by mutations in the CYBB gene, the condition is inherited in an X-linked recessive pattern. When chronic granulomatous disease is caused by CYBA, NCF1, NCF2, or NCF4 gene mutations, the condition is inherited in an autosomal recessive pattern.
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
Disease having a short and relatively severe course.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
DEFENSINS found in azurophilic granules of neutrophils and in the secretory granules of intestinal PANETH CELLS.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Role of Listeria monocytogenes exotoxins listeriolysin and phosphatidylinositol-specific phospholipase C in activation of human neutrophils. (1/1266)

Polymorphonuclear leukocytes (PMN) are essential for resolution of infections with Listeria monocytogenes. The present study investigated the role of the listerial exotoxins listeriolysin (LLO) and phosphatidylinositol-specific phospholipase C (PlcA) in human neutrophil activation. Different Listeria strains, mutated in individual virulence genes, as well as purified LLO were used. Coincubation of human neutrophils with wild-type L. monocytogenes provoked PMN activation, occurring independently of phagocytosis events, with concomitant elastase secretion, leukotriene generation, platelet-activating factor (PAF) synthesis, respiratory burst, and enhanced phosphoinositide hydrolysis. Degranulation and leukotriene formation were noted to be solely dependent on LLO expression, as these features were absent when the LLO-defective mutant EGD- and the avirulent strain L. innocua were used. These effects were fully reproduced by a recombinant L. innocua strain expressing LLO (INN+) and by the purified LLO molecule. LLO secretion was also required for PAF synthesis. However, wild-type L. monocytogenes was more potent in eliciting PAF formation than mutants expressing LLO, suggesting the involvement of additional virulence factors. This was even more obvious for phosphoinositide hydrolysis and respiratory burst: these events were provoked not only by INN+ but also by the LLO-defective mutant EGD- and by a recombinant L. innocua strain producing listerial PlcA. We conclude that human neutrophils react to extracellularly provided listerial exotoxins by rapid cell activation. Listeriolysin is centrally involved in triggering degranulation and lipid mediator generation, and further virulence factors such as PlcA apparently contribute to trigger neutrophil phosphoinositide hydrolysis and respiratory burst. In this way, listerial exotoxins may influence the host defense against infections with L. monocytogenes.  (+info)

Does soluble intercellular adhesion molecule-1 (ICAM-1) affect neutrophil activation and adhesion following ischaemia-reperfusion? (2/1266)

OBJECTIVES: To examine the effect of reperfusion plasma and sICAM-1 on neutrophil integrin expression and neutrophil adhesion to determine if sICAM-1 has a potential role in the regulation of neutrophil adhesion. MATERIALS: Twenty-seven patients, 17 men and 10 women undergoing femorodistal surgery. Blood was taken preoperatively and from the femoral vein following the release of the cross-clamp. Neutrophils were obtained from five volunteers and incubated with phosphate buffered saline (PBS), preoperative plasma or reperfusion plasma with and without sICAM-1. Neutrophil expression of CD11b and adhesion were measured. MAIN RESULTS: Neutrophil CD11b expression did not change following incubation in the three media. Neutrophil adhesion increased significantly following exposure to reperfusion plasma compared to PBS or preoperative plasma (45.5 adhesion vs. 12.75%, p < 0.01 Mann-Whitney U-test). Soluble ICAM-1 decreased CD11b expression and adhesion in neutrophils exposed to reperfusion plasma only (CD11b expression fell from 15.9 to 3.4 mcf, p < 0.01 Mann-Whitney U-test and adhesion fell to 11.6% cells adhered, p < 0.01). CONCLUSION: An increase in CD11b expression is not required for an increase in neutrophil adhesion. The change in neutrophil adhesion produced by reperfusion plasma can be blocked by sICAM-1. Soluble ICAM-1 may have a physiological role in the regulation of neutrophil adhesion.  (+info)

Mechanisms of acute inflammatory lung injury induced by abdominal sepsis. (3/1266)

Sequestration of neutrophils and release of histotoxic mediators are considered important for the development of pathologic alterations of the lung defined as adult respiratory distress syndrome. Mechanisms of inflammatory lung injury caused by abdominal sepsis were investigated using the colon ascendens stent peritonitis (CASP) model that closely mimics the human disease. In the CASP model, a continuous leakage of intraluminal bacteria into the peritoneal cavity is induced by implantation of a stent in the ascending colon, generating a septic focus. In contrast to the cecal ligation and puncture model of peritonitis, survival of mice following CASP surgery is dependent on IFN-gamma, but independent of tumor necrosis factor (TNF). Here we show that the systemic inflammation induced by CASP surgery results in a rapid and profound increase of lung vascular permeability that was associated with the activation and recruitment of neutrophils to the lung. Activation of circulating granulocytes was characterized by increased production of serine proteinases and reactive oxygen metabolites, as well as elevated expression of cell surface Mac-1. Expression of MIP-2, KC, MIP-1alpha and E-selectin mRNA in lung was strongly increased within 3 h following CASP surgery, whereas up-regulation of IP-10, MCP-1 and P-selectin was delayed. In contrast, induction of RANTES, LIX, ICAM-1 and VCAM-1 mRNA was weak or not detectable after CASP surgery. Importantly, recruitment of leukocytes to the lung was normal in lipopolysaccharide-resistant mice, and was not affected by antibody neutralization of TNF or the chemokines MIP-2 and KC.  (+info)

Mediators of anaphylaxis but not activated neutrophils augment cholinergic responses of equine small airways. (4/1266)

Neutrophilic inflammation in small airways (SA) and bronchospasm mediated via muscarinic receptors are features of chronic obstructive pulmonary disease in horses (COPD). Histamine, serotonin, and leukotrienes (LTs) are reported to be involved in the exacerbation of COPD, and currently, histamine has been shown to increase tension response to electrical field simulation (EFS) in equine SA. We tested the effects of these mediators and the effects of activated neutrophils on the cholinergic responses in SA. Histamine, serotonin, and LTD4 had a synergistic effect on EFS responses and only an additive effect on the tension response to exogenous ACh or methacholine. Atropine and TTX entirely eliminated the EFS-induced tension response in the presence of all three inflammatory mediators, indicating that augmentation of the EFS response applies only to the endogenous cholinergic response. Neutrophils isolated from control and COPD-affected horses were activated by zymosan, producing 18.1 +/- 2.3 and 25.0 +/- 2.3 nmol superoxide. 10(6) cells-1. 30 min-1, respectively. However, in contrast to the profound effect of mediators, incubation of SA for over 1 h in a suspension of up to 30 x 10(6) zymosan-treated neutrophils/ml did not significantly affect EFS responses of SA isolated from either control or COPD-affected horses. We conclude that in equine SA 1) the endogenous cholinergic responses are subject to strong facilitation by inflammatory mediators; 2) activated neutrophils do not affect cholinergic responses in SA; and 3) in acute bouts of equine COPD, histamine, LTD4, and serotonin (mediators primarily associated with type I allergic reaction) rather than mediators derived from neutrophils most likely contribute to increased cholinergic airway tone.  (+info)

Morphine preconditioning attenuates neutrophil activation in rat models of myocardial infarction. (5/1266)

Previous results from our laboratory have suggested that morphine can attenuate neutrophil activation in patients with acute myocardial infarction. To elucidate if morphine preconditioning (PC) has the same effects via activation of neutrophil endopeptidase 24.11 (NEP), we measured serum levels of intercellular adhesion molecule-1 (ICAM-1), gp100MEL14 and NEP in adult Wistar rats subjected to ten different protocols (n = 10 for each) at baseline, immediately after and 2 h after morphine PC. All groups were subjected to 30 min of occlusion and 2 h of reperfusion. Similarly, morphine-induced PC was elicited by 3-min drug infusions (100 micrograms/kg) interspersed with 5-min drug-free periods before the prolonged 30-min occlusion. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by triphenyltetrazolium staining. Pretreatment with morphine increased NEP activities (9.86 +/- 1.98 vs. 5.12 +/- 1.10 nmol/mg protein in control group; p < 0.001). Naloxone (mu-opioid receptor antagonist) (4.82 +/- 1.02 nmol/mg protein) and phosphoramidon (NEP inhibitor) (4.66 +/- 1.00 nmol/mg protein) inhibited morphine-activated NEP, whereas glibenclamide (ATP-sensitive potassium channel antagonist) and chelerythrine (protein kinase C inhibitor) had no effects. The ICAM-1 and gp100MEL14 of the third sampling were lowest for those with morphine PC (280 +/- 30 ng/ml and 2.2 +/- 0.7 micrograms/ml; p < 0.001), but naloxone (372 +/- 38 ng/ml and 3.8 +/- 0.9 micrograms/ml) and phosphoramidon (382 +/- 40 ng/ml and 4.2 +/- 1.1 micrograms/ml) abolished the above phenomenon. IS/AAR were definitely lowest for those with morphine PC (24 +/- 7%; p < 0.05). Morphine preconditioning increases NEP activities to attenuate shedding of gp100MEL14 and to ICAM-1 and, thus, provides myocardial protection.  (+info)

A functional granulocyte colony-stimulating factor receptor is required for normal chemoattractant-induced neutrophil activation. (6/1266)

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor that is widely used to treat neutropenia. In addition to stimulating polymorphonuclear neutrophil (PMN) production, G-CSF may have significant effects on PMN function. Because G-CSF receptor (G-CSFR)-deficient mice do not have the expected neutrophilia after administration of human interleukin-8 (IL-8), we examined the effect of the loss of G-CSFR on IL-8-stimulated PMN function. Compared with wild-type PMNs, PMNs isolated from G-CSFR-deficient mice demonstrated markedly decreased chemotaxis to IL-8. PMN emigration into the skin of G-CSFR-deficient mice in response to IL-8 was also impaired. Significant chemotaxis defects were also seen in response to N-formyl-methionyl-leucyl-phenylalanine, zymosan-activated serum, or macrophage inflammatory protein-2. The defective chemotactic response to IL-8 does not appear to be due to impaired chemoattractant receptor function, as the number of IL-8 receptors and chemoattractant-induced calcium influx, actin polymerization, and release of gelatinase B were comparable to those of wild-type PMNs. Chemoattractant-induced adhesion of G-CSFR-deficient PMNs was significantly impaired, suggesting a defect in beta2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation are present in G-CSFR-deficient mice and indicate that G-CSF plays an important role in regulating PMN chemokine responsiveness.  (+info)

P-selectin mediates neutrophil adhesion to endothelial cell borders. (7/1266)

During an acute inflammatory response, endothelial P-selectin (CD62P) can mediate the initial capture of neutrophils from the free flowing bloodstream. P-selectin is stored in secretory granules (Weibel-Palade bodies) and is rapidly expressed on the endothelial surface after stimulation with histamine or thrombin. Because neutrophil transmigration occurs preferentially at endothelial borders, we wished to determine whether P-selectin-dependent neutrophil capture (adhesion) occurs at endothelial cell borders. Under static or hydrodynamic flow (2 dyn/cm2) conditions, histamine (10(-4) M) or thrombin (0.2 U/mL) treatment induced preferential (> or = 75%) neutrophil adhesion to the cell borders of endothelial monolayers. Blocking antibody studies established that neutrophil adhesion was completely P-selectin dependent. P-selectin surface expression increased significantly after histamine treatment and P-selectin immunostaining was concentrated along endothelial borders. We conclude that preferential P-selectin expression along endothelial borders may be an important mechanism for targeting neutrophil migration at endothelial borders.  (+info)

Antibodies to CD18 influence neutrophil migration through extracellular matrix. (8/1266)

Mac-1 (CD11b/CD18) is known to be involved in neutrophil (PMN) adhesion to endothelial cells and extracellular matrix. Although antibodies to CD 18 are being tested for therapy in humans, their role in PMN migration through the extracellular matrix is unknown. We used direct visualization to quantify PMN motility through reconstituted, three-dimensional gels of collagen type I. Gels were prepared with different concentrations of collagen (ranging from 0.1 to 1.0 mg/mL) and PMN migration was examined in the presence and absence of antibodies to CD18 (anti-CD18), with and without stimulation by N-formyl peptides. In low-concentration gels (<0.6 mg/mL), anti-CD18 had a significant influence on PMN migration, increasing motility in unstimulated PMN by 90% at 0.3 mg/mL collagen, and decreasing motility in N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated PMN by 70% at 0.4 mg/mL collagen. But antiCD18 had no effect on the rate of cell migration through high-concentration collagen gels (>0.6 mg/mL). PMN migration through collagen gels is CD18-dependent but only under conditions of high hydration, suggesting that CD18-mediated effects (e.g., adhesion to gel fibers) are only important when the fiber density is relatively low. Anti-CD18 inhibited, but did not eliminate, the adhesion of fMLP-stimulated PMN to the surface of collagen gels, suggesting that cells use multiple mechanisms for gaining traction within the gel. Because of the multiple modes of interaction between motile cells and the deformable fiber matrix, blockade of one component, such as CD18, can enhance the rate of cell migration under one set of conditions, and inhibit under another.  (+info)

Neutrophil activation refers to the process by which neutrophils, a type of white blood cell, become activated in response to a signal or stimulus, such as an infection or inflammation. This activation triggers a series of responses within the neutrophil that enable it to carry out its immune functions, including:

1. Degranulation: The release of granules containing enzymes and other proteins that can destroy microbes.
2. Phagocytosis: The engulfment and destruction of microbes through the use of reactive oxygen species (ROS) and other toxic substances.
3. Formation of neutrophil extracellular traps (NETs): A process in which neutrophils release DNA and proteins to trap and kill microbes outside the cell.
4. Release of cytokines and chemokines: Signaling molecules that recruit other immune cells to the site of infection or inflammation.

Neutrophil activation is a critical component of the innate immune response, but excessive or uncontrolled activation can contribute to tissue damage and chronic inflammation.

Neutrophils are a type of white blood cell that are part of the immune system's response to infection. They are produced in the bone marrow and released into the bloodstream where they circulate and are able to move quickly to sites of infection or inflammation in the body. Neutrophils are capable of engulfing and destroying bacteria, viruses, and other foreign substances through a process called phagocytosis. They are also involved in the release of inflammatory mediators, which can contribute to tissue damage in some cases. Neutrophils are characterized by the presence of granules in their cytoplasm, which contain enzymes and other proteins that help them carry out their immune functions.

N-Formylmethionine Leucyl-Phenylalanine (fMLP) is not a medical condition, but rather a synthetic peptide that is often used in laboratory settings for research purposes. It is a formylated methionine residue linked to a leucine and phenylalanine tripeptide.

fMLP is a potent chemoattractant for certain types of white blood cells, including neutrophils and monocytes. When these cells encounter fMLP, they are stimulated to migrate towards the source of the peptide and release various inflammatory mediators. As such, fMLP is often used in studies of inflammation, immune cell function, and signal transduction pathways.

It's important to note that while fMLP has important research applications, it is not a substance that would be encountered or used in clinical medicine.

Neutrophil infiltration is a pathological process characterized by the accumulation of neutrophils, a type of white blood cell, in tissue. It is a common feature of inflammation and occurs in response to infection, injury, or other stimuli that trigger an immune response. Neutrophils are attracted to the site of tissue damage by chemical signals called chemokines, which are released by damaged cells and activated immune cells. Once they reach the site of inflammation, neutrophils help to clear away damaged tissue and microorganisms through a process called phagocytosis. However, excessive or prolonged neutrophil infiltration can also contribute to tissue damage and may be associated with various disease states, including cancer, autoimmune disorders, and ischemia-reperfusion injury.

Peroxidase is a type of enzyme that catalyzes the chemical reaction in which hydrogen peroxide (H2O2) is broken down into water (H2O) and oxygen (O2). This enzymatic reaction also involves the oxidation of various organic and inorganic compounds, which can serve as electron donors.

Peroxidases are widely distributed in nature and can be found in various organisms, including bacteria, fungi, plants, and animals. They play important roles in various biological processes, such as defense against oxidative stress, breakdown of toxic substances, and participation in metabolic pathways.

The peroxidase-catalyzed reaction can be represented by the following chemical equation:

H2O2 + 2e- + 2H+ → 2H2O

In this reaction, hydrogen peroxide is reduced to water, and the electron donor is oxidized. The peroxidase enzyme facilitates the transfer of electrons between the substrate (hydrogen peroxide) and the electron donor, making the reaction more efficient and specific.

Peroxidases have various applications in medicine, industry, and research. For example, they can be used for diagnostic purposes, as biosensors, and in the treatment of wastewater and medical wastes. Additionally, peroxidases are involved in several pathological conditions, such as inflammation, cancer, and neurodegenerative diseases, making them potential targets for therapeutic interventions.

Respiratory burst is a term used in the field of biology, particularly in the context of immunology and cellular processes. It does not have a direct application to clinical medicine, but it is important for understanding certain physiological and pathophysiological mechanisms. Here's a definition of respiratory burst:

Respiratory burst is a rapid increase in oxygen consumption by phagocytic cells (like neutrophils, monocytes, and macrophages) following their activation in response to various stimuli, such as pathogens or inflammatory molecules. This process is part of the innate immune response and serves to eliminate invading microorganisms.

The respiratory burst involves the activation of NADPH oxidase, an enzyme complex present in the membrane of phagosomes (the compartment where pathogens are engulfed). Upon activation, NADPH oxidase catalyzes the reduction of oxygen to superoxide radicals, which then dismutate to form hydrogen peroxide. These reactive oxygen species (ROS) can directly kill or damage microorganisms and also serve as signaling molecules for other immune cells.

While respiratory burst is a crucial part of the immune response, excessive or dysregulated ROS production can contribute to tissue damage and chronic inflammation, which have implications in various pathological conditions, such as atherosclerosis, neurodegenerative diseases, and cancer.

The Macrophage-1 Antigen (also known as Macrophage Antigen-1 or CD14) is a glycoprotein found on the surface of various cells, including monocytes, macrophages, and some dendritic cells. It functions as a receptor for complexes formed by lipopolysaccharides (LPS) and LPS-binding protein (LBP), which are involved in the immune response to gram-negative bacteria. CD14 plays a crucial role in activating immune cells and initiating the release of proinflammatory cytokines upon recognizing bacterial components.

In summary, Macrophage-1 Antigen is a cell surface receptor that contributes to the recognition and response against gram-negative bacteria by interacting with LPS-LBP complexes.

Superoxides are partially reduced derivatives of oxygen that contain one extra electron, giving them an overall charge of -1. They are highly reactive and unstable, with the most common superoxide being the hydroxyl radical (•OH-) and the superoxide anion (O2-). Superoxides are produced naturally in the body during metabolic processes, particularly within the mitochondria during cellular respiration. They play a role in various physiological processes, but when produced in excess or not properly neutralized, they can contribute to oxidative stress and damage to cells and tissues, potentially leading to the development of various diseases such as cancer, atherosclerosis, and neurodegenerative disorders.

Chemotaxis, Leukocyte is the movement of leukocytes (white blood cells) towards a higher concentration of a particular chemical substance, known as a chemotactic factor. This process plays a crucial role in the immune system's response to infection and injury.

When there is an infection or tissue damage, certain cells release chemotactic factors, which are small molecules or proteins that can attract leukocytes to the site of inflammation. Leukocytes have receptors on their surface that can detect these chemotactic factors and move towards them through a process called chemotaxis.

Once they reach the site of inflammation, leukocytes can help eliminate pathogens or damaged cells by phagocytosis (engulfing and destroying) or releasing toxic substances that kill the invading microorganisms. Chemotaxis is an essential part of the immune system's defense mechanisms and helps to maintain tissue homeostasis and prevent the spread of infection.

CD18 is a type of protein called an integrin that is found on the surface of many different types of cells in the human body, including white blood cells (leukocytes). It plays a crucial role in the immune system by helping these cells to migrate through blood vessel walls and into tissues where they can carry out their various functions, such as fighting infection and inflammation.

CD18 forms a complex with another protein called CD11b, and together they are known as Mac-1 or CR3 (complement receptor 3). This complex is involved in the recognition and binding of various molecules, including bacterial proteins and fragments of complement proteins, which help to trigger an immune response.

CD18 has been implicated in a number of diseases, including certain types of cancer, inflammatory bowel disease, and rheumatoid arthritis. Mutations in the gene that encodes CD18 can lead to a rare disorder called leukocyte adhesion deficiency (LAD) type 1, which is characterized by recurrent bacterial infections and impaired wound healing.

CD11b, also known as integrin αM or Mac-1, is not an antigen itself but a protein that forms part of a family of cell surface receptors called integrins. These integrins play a crucial role in various biological processes, including cell adhesion, migration, and signaling.

CD11b combines with CD18 (integrin β2) to form the heterodimeric integrin αMβ2, also known as Mac-1 or CR3 (complement receptor 3). This integrin is primarily expressed on the surface of myeloid cells, such as monocytes, macrophages, and neutrophils.

As an integral part of the immune system, CD11b/CD18 recognizes and binds to various ligands, including:

1. Icosahedral bacterial components like lipopolysaccharides (LPS) and peptidoglycans
2. Fragments of complement component C3b (iC3b)
3. Fibrinogen and other extracellular matrix proteins
4. Certain immune cell receptors, such as ICAM-1 (intercellular adhesion molecule 1)

The binding of CD11b/CD18 to these ligands triggers various intracellular signaling pathways that regulate the immune response and inflammation. In this context, antigens are substances (usually proteins or polysaccharides) found on the surface of cells, viruses, or bacteria that can be recognized by the immune system. CD11b/CD18 plays a role in recognizing and responding to these antigens during an immune response.

Cell degranulation is the process by which cells, particularly immune cells like mast cells and basophils, release granules containing inflammatory mediators in response to various stimuli. These mediators include histamine, leukotrienes, prostaglandins, and other chemicals that play a role in allergic reactions, inflammation, and immune responses. The activation of cell surface receptors triggers a signaling cascade that leads to the exocytosis of these granules, resulting in degranulation. This process is important for the immune system's response to foreign invaders and for the development of allergic reactions.

Myeloblastin is not typically used as a medical term in current literature. However, in the field of hematology, "myeloblast" refers to an immature cell that develops into a white blood cell called a granulocyte. These myeloblasts are normally found in the bone marrow and are part of the body's immune system.

If you meant 'Myeloperoxidase,' I can provide a definition for it:

Myeloperoxidase (MPO) is a peroxidase enzyme that is abundant in neutrophil granulocytes, a type of white blood cell involved in the immune response. MPO plays an essential role in the microbicidal activity of these cells by generating hypochlorous acid and other reactive oxygen species to kill invading pathogens.

L-Selectin, also known as LECAM-1 (Leukocyte Cell Adhesion Molecule 1), is a type of cell adhesion molecule that is found on the surface of leukocytes (white blood cells). It plays an important role in the immune system by mediating the initial attachment and rolling of leukocytes along the endothelial lining of blood vessels, which is a critical step in the process of inflammation and immune response.

L-Selectin recognizes specific sugar structures called sialyl Lewis x (sLeX) and related structures on the surface of endothelial cells, allowing leukocytes to bind to them. This interaction helps to slow down the leukocytes and facilitate their extravasation from the blood vessels into the surrounding tissues, where they can carry out their immune functions.

L-Selectin is involved in a variety of immunological processes, including the recruitment of leukocytes to sites of infection or injury, the homing of lymphocytes to lymphoid organs, and the regulation of immune cell trafficking under homeostatic conditions.

Interleukin-8 (IL-8) is a type of cytokine, which is a small signaling protein involved in immune response and inflammation. IL-8 is also known as neutrophil chemotactic factor or NCF because it attracts neutrophils, a type of white blood cell, to the site of infection or injury.

IL-8 is produced by various cells including macrophages, epithelial cells, and endothelial cells in response to bacterial or inflammatory stimuli. It acts by binding to specific receptors called CXCR1 and CXCR2 on the surface of neutrophils, which triggers a series of intracellular signaling events leading to neutrophil activation, migration, and degranulation.

IL-8 plays an important role in the recruitment of neutrophils to the site of infection or tissue damage, where they can phagocytose and destroy invading microorganisms. However, excessive or prolonged production of IL-8 has been implicated in various inflammatory diseases such as chronic obstructive pulmonary disease (COPD), rheumatoid arthritis, and cancer.

Pancreatic elastase is a type of elastase that is specifically produced by the pancreas. It is an enzyme that helps in digesting proteins found in the food we eat. Pancreatic elastase breaks down elastin, a protein that provides elasticity to tissues and organs in the body.

In clinical practice, pancreatic elastase is often measured in stool samples as a diagnostic tool to assess exocrine pancreatic function. Low levels of pancreatic elastase in stool may indicate malabsorption or exocrine pancreatic insufficiency, which can be caused by various conditions such as chronic pancreatitis, cystic fibrosis, or pancreatic cancer.

Antineutrophil cytoplasmic antibodies (ANCAs) are a type of autoantibody that specifically target certain proteins in the cytoplasm of neutrophils, which are a type of white blood cell. These antibodies are associated with several types of vasculitis, which is inflammation of the blood vessels.

There are two main types of ANCAs: perinuclear ANCAs (p-ANCAs) and cytoplasmic ANCAs (c-ANCAs). p-ANCAs are directed against myeloperoxidase, a protein found in neutrophil granules, while c-ANCAs target proteinase 3, another protein found in neutrophil granules.

The presence of ANCAs in the blood can indicate an increased risk for developing certain types of vasculitis, such as granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA). ANCA testing is often used in conjunction with other clinical findings to help diagnose and manage these conditions.

It's important to note that while the presence of ANCAs can indicate an increased risk for vasculitis, not everyone with ANCAs will develop the condition. Additionally, ANCAs can also be found in some individuals without any associated disease, so their presence should be interpreted in the context of other clinical findings.

Chemotactic factors are substances that attract or repel cells, particularly immune cells, by stimulating directional movement in response to a chemical gradient. These factors play a crucial role in the body's immune response and inflammation process. They include:

1. Chemokines: A family of small signaling proteins that direct the migration of immune cells to sites of infection or tissue damage.
2. Cytokines: A broad category of signaling molecules that mediate and regulate immunity, inflammation, and hematopoiesis. Some cytokines can also act as chemotactic factors.
3. Complement components: Cleavage products of the complement system can attract immune cells to the site of infection or tissue injury.
4. Growth factors: Certain growth factors, like colony-stimulating factors (CSFs), can stimulate the migration and proliferation of specific cell types.
5. Lipid mediators: Products derived from arachidonic acid metabolism, such as leukotrienes and prostaglandins, can also act as chemotactic factors.
6. Formyl peptides: Bacterial-derived formylated peptides can attract and activate neutrophils during an infection.
7. Extracellular matrix (ECM) components: Fragments of ECM proteins, like collagen and fibronectin, can serve as chemotactic factors for immune cells.

These factors help orchestrate the immune response by guiding the movement of immune cells to specific locations in the body where they are needed.

Complement C5a is a protein fragment that is generated during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by tagging them for destruction and attracting immune cells to the site of infection or injury.

C5a is formed when the fifth component of the complement system (C5) is cleaved into two smaller fragments, C5a and C5b, during the complement activation cascade. C5a is a potent pro-inflammatory mediator that can attract and activate various immune cells, such as neutrophils, monocytes, and eosinophils, to the site of infection or injury. It can also increase vascular permeability, promote the release of histamine, and induce the production of reactive oxygen species, all of which contribute to the inflammatory response.

However, excessive or uncontrolled activation of the complement system and generation of C5a can lead to tissue damage and inflammation, contributing to the pathogenesis of various diseases, such as sepsis, acute respiratory distress syndrome (ARDS), and autoimmune disorders. Therefore, targeting C5a or its receptors has been explored as a potential therapeutic strategy for these conditions.

Leukocyte elastase is a type of enzyme that is released by white blood cells (leukocytes), specifically neutrophils, during inflammation. Its primary function is to help fight infection by breaking down the proteins in bacteria and viruses. However, if not properly regulated, leukocyte elastase can also damage surrounding tissues, contributing to the progression of various diseases such as chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), and cystic fibrosis.

Leukocyte elastase is often measured in clinical settings as a marker of inflammation and neutrophil activation, particularly in patients with lung diseases. Inhibitors of leukocyte elastase have been developed as potential therapeutic agents for these conditions.

Decompression sickness (DCS), also known as "the bends," is a medical condition that results from dissolved gases coming out of solution in the body's tissues and forming bubbles during decompression. This typically occurs when a person who has been exposed to increased pressure at depth, such as scuba divers or compressed air workers, ascends too quickly.

The elevated pressure at depth causes nitrogen to dissolve into the blood and tissues of the body. As the diver ascends and the pressure decreases, the dissolved gases form bubbles, which can cause symptoms ranging from joint pain and rashes to paralysis and death. The risk of DCS is influenced by several factors, including depth, duration of exposure, rate of ascent, and individual susceptibility.

Prevention of DCS involves following established dive tables or using a personal decompression computer to calculate safe ascent rates and decompression stops. Additionally, proper hydration, fitness, and avoiding alcohol and tobacco before diving can reduce the risk of DCS. Treatment typically involves administering oxygen and recompression therapy in a hyperbaric chamber.

Cell adhesion refers to the binding of cells to extracellular matrices or to other cells, a process that is fundamental to the development, function, and maintenance of multicellular organisms. Cell adhesion is mediated by various cell surface receptors, such as integrins, cadherins, and immunoglobulin-like cell adhesion molecules (Ig-CAMs), which interact with specific ligands in the extracellular environment. These interactions lead to the formation of specialized junctions, such as tight junctions, adherens junctions, and desmosomes, that help to maintain tissue architecture and regulate various cellular processes, including proliferation, differentiation, migration, and survival. Disruptions in cell adhesion can contribute to a variety of diseases, including cancer, inflammation, and degenerative disorders.

Formyl peptide receptors (FPRs) are a type of G protein-coupled receptors that play a crucial role in the innate immune system. They are expressed on various cells including neutrophils, monocytes, and macrophages. FPRs recognize and respond to formylated peptides derived from bacteria, mitochondria, and host proteins during cell damage or stress. Activation of FPRs triggers a variety of cellular responses, such as chemotaxis, phagocytosis, and release of inflammatory mediators, which help to eliminate invading pathogens and promote tissue repair. There are three subtypes of human FPRs (FPR1, FPR2, and FPR3) that have distinct ligand specificities and functions in the immune response.

Luminescent measurements refer to the quantitative assessment of the emission of light from a substance that has been excited, typically through some form of energy input such as electrical energy or radiation. In the context of medical diagnostics and research, luminescent measurements can be used in various applications, including bioluminescence imaging, which is used to study biological processes at the cellular and molecular level.

Bioluminescence occurs when a chemical reaction produces light within a living organism, often through the action of enzymes such as luciferase. By introducing a luciferase gene into cells or organisms, researchers can use bioluminescent measurements to track cellular processes and monitor gene expression in real time.

Luminescent measurements may also be used in medical research to study the properties of materials used in medical devices, such as LEDs or optical fibers, or to develop new diagnostic tools based on light-emitting nanoparticles or other luminescent materials.

In summary, luminescent measurements are a valuable tool in medical research and diagnostics, providing a non-invasive way to study biological processes and develop new technologies for disease detection and treatment.

Phagocytosis is the process by which certain cells in the body, known as phagocytes, engulf and destroy foreign particles, bacteria, or dead cells. This mechanism plays a crucial role in the immune system's response to infection and inflammation. Phagocytes, such as neutrophils, monocytes, and macrophages, have receptors on their surface that recognize and bind to specific molecules (known as antigens) on the target particles or microorganisms.

Once attached, the phagocyte extends pseudopodia (cell extensions) around the particle, forming a vesicle called a phagosome that completely encloses it. The phagosome then fuses with a lysosome, an intracellular organelle containing digestive enzymes and other chemicals. This fusion results in the formation of a phagolysosome, where the engulfed particle is broken down by the action of these enzymes, neutralizing its harmful effects and allowing for the removal of cellular debris or pathogens.

Phagocytosis not only serves as a crucial defense mechanism against infections but also contributes to tissue homeostasis by removing dead cells and debris.

Leukotriene B4 (LTB4) is a type of lipid mediator called eicosanoid, which is derived from arachidonic acid through the 5-lipoxygenase pathway. It is primarily produced by neutrophils, eosinophils, monocytes, and macrophages in response to various stimuli such as infection, inflammation, or injury. LTB4 acts as a potent chemoattractant and activator of these immune cells, playing a crucial role in the recruitment and activation of neutrophils during acute inflammatory responses. It also enhances the adhesion of leukocytes to endothelial cells, contributing to the development of tissue damage and edema. Dysregulation of LTB4 production has been implicated in several pathological conditions, including asthma, atherosclerosis, and cancer.

Lactoferrin is a glycoprotein that belongs to the transferrin family. It is an iron-binding protein found in various exocrine secretions such as milk, tears, and saliva, as well as in neutrophils, which are a type of white blood cell involved in immune response. Lactoferrin plays a role in iron homeostasis, antimicrobial activity, and anti-inflammatory responses. It has the ability to bind free iron, which can help prevent bacterial growth by depriving them of an essential nutrient. Additionally, lactoferrin has been shown to have direct antimicrobial effects against various bacteria, viruses, and fungi. Its role in the immune system also includes modulating the activity of immune cells and regulating inflammation.

Chemokine (C-X-C motif) ligand 1 (CXCL1), also known as growth-regulated oncogene-alpha (GRO-α), is a small signaling protein belonging to the chemokine family. Chemokines are a group of cytokines, or cell signaling molecules, that play important roles in immune responses and inflammation by recruiting immune cells to sites of infection or tissue injury.

CXCL1 specifically binds to and activates the CXCR2 receptor, which is found on various types of immune cells, such as neutrophils, monocytes, and lymphocytes. The activation of the CXCR2 receptor by CXCL1 leads to a series of intracellular signaling events that result in the directed migration of these immune cells towards the site of chemokine production.

CXCL1 is involved in various physiological and pathological processes, including wound healing, angiogenesis, and tumor growth and metastasis. It has been implicated in several inflammatory diseases, such as rheumatoid arthritis, psoriasis, and atherosclerosis, as well as in cancer progression and metastasis.

Interleukin-8 (IL-8) receptors are a type of cell surface receptor that bind to and are activated by the cytokine IL-8. There are two main types of IL-8 receptors, known as CXCR1 and CXCR2. Both of these receptors belong to the G protein-coupled receptor (GPCR) family and play important roles in the immune response, particularly in the recruitment and activation of neutrophils, a type of white blood cell that helps to fight infection.

IL-8A, also known as CXCR1, is a specific subtype of IL-8 receptor. It is a 354-amino acid protein that is expressed on the surface of many different types of cells, including neutrophils, monocytes, and certain tumor cells. When IL-8 binds to CXCR1, it activates a variety of signaling pathways within the cell that lead to changes in gene expression, cell activation, and chemotaxis (directed movement) towards the source of IL-8.

CXCR1 plays an important role in the immune response to bacterial and fungal infections, as well as in the development and progression of certain inflammatory diseases and cancers. It is also a target for drug development, particularly in the areas of cancer therapy and inflammatory disease.

Tetradecanoylphorbol acetate (TPA) is defined as a pharmacological agent that is a derivative of the phorbol ester family. It is a potent tumor promoter and activator of protein kinase C (PKC), a group of enzymes that play a role in various cellular processes such as signal transduction, proliferation, and differentiation. TPA has been widely used in research to study PKC-mediated signaling pathways and its role in cancer development and progression. It is also used in topical treatments for skin conditions such as psoriasis.

Zymosan is a type of substance that is derived from the cell walls of yeast and some types of fungi. It's often used in laboratory research as an agent to stimulate inflammation, because it can activate certain immune cells (such as neutrophils) and cause them to release pro-inflammatory chemicals.

In medical terms, Zymosan is sometimes used as a tool for studying the immune system and inflammation in experimental settings. It's important to note that Zymosan itself is not a medical condition or disease, but rather a research reagent with potential applications in understanding human health and disease.

IgG receptors, also known as Fcγ receptors (Fc gamma receptors), are specialized protein molecules found on the surface of various immune cells, such as neutrophils, monocytes, macrophages, and some lymphocytes. These receptors recognize and bind to the Fc region of IgG antibodies, one of the five classes of immunoglobulins in the human body.

IgG receptors play a crucial role in immune responses by mediating different effector functions, including:

1. Antibody-dependent cellular cytotoxicity (ADCC): IgG receptors on natural killer (NK) cells and other immune cells bind to IgG antibodies coated on the surface of virus-infected or cancer cells, leading to their destruction.
2. Phagocytosis: When IgG antibodies tag pathogens or foreign particles, phagocytes like neutrophils and macrophages recognize and bind to these immune complexes via IgG receptors, facilitating the engulfment and removal of the targeted particles.
3. Antigen presentation: IgG receptors on antigen-presenting cells (APCs) can internalize immune complexes, process the antigens, and present them to T cells, thereby initiating adaptive immune responses.
4. Inflammatory response regulation: IgG receptors can modulate inflammation by activating or inhibiting downstream signaling pathways in immune cells, depending on the specific type of Fcγ receptor and its activation state.

There are several types of IgG receptors (FcγRI, FcγRII, FcγRIII, and FcγRIV) with varying affinities for different subclasses of IgG antibodies (IgG1, IgG2, IgG3, and IgG4). The distinct functions and expression patterns of these receptors contribute to the complexity and fine-tuning of immune responses in the human body.

Inflammation is a complex biological response of tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is characterized by the following signs: rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). The process involves the activation of the immune system, recruitment of white blood cells, and release of inflammatory mediators, which contribute to the elimination of the injurious stimuli and initiation of the healing process. However, uncontrolled or chronic inflammation can also lead to tissue damage and diseases.

A leukocyte count, also known as a white blood cell (WBC) count, is a laboratory test that measures the number of leukocytes in a sample of blood. Leukocytes are a vital part of the body's immune system and help fight infection and inflammation. A high or low leukocyte count may indicate an underlying medical condition, such as an infection, inflammation, or a bone marrow disorder. The normal range for a leukocyte count in adults is typically between 4,500 and 11,000 cells per microliter (mcL) of blood. However, the normal range can vary slightly depending on the laboratory and the individual's age and sex.

Beta-thromboglobulin is a type of protein that is released from platelets (a component of blood) when they are activated. It is often used as a marker for platelet activation, which can occur in various physiological and pathological conditions such as hemostasis, thrombosis, inflammation, and atherosclerosis.

Beta-thromboglobulin is a member of the thromboglobulin family, which also includes platelet factor 4 (PF4) and other proteins that are involved in hemostasis and thrombosis. These proteins play important roles in the regulation of blood clotting and wound healing, but their excessive release or activation can contribute to the development of various cardiovascular diseases, such as myocardial infarction (heart attack) and stroke.

Elevated levels of beta-thromboglobulin have been found in patients with thromboembolic disorders, inflammatory bowel disease, cancer, and other conditions associated with platelet activation. Therefore, the measurement of beta-thromboglobulin can be useful in the diagnosis and monitoring of these diseases.

Calcium pyrophosphate is a mineral compound made up of calcium and pyrophosphate ions. In the body, it can form crystals that deposit in joints, causing a type of arthritis known as calcium pyrophosphate deposition (CPPD) disease or pseudogout. CPPD disease is characterized by sudden attacks of joint pain and swelling, often in the knee or wrist. The condition is more common in older adults and can also occur in people with underlying medical conditions such as hyperparathyroidism, hemochromatosis, and hypophosphatasia. Calcium pyrophosphate crystals may also be found in the fluid around the heart (pericardial fluid) or in other tissues, but they do not always cause symptoms.

Cytochalasin B is a fungal metabolite that inhibits actin polymerization in cells, which can disrupt the cytoskeleton and affect various cellular processes such as cell division and motility. It is often used in research to study actin dynamics and cell shape.

Lipopolysaccharides (LPS) are large molecules found in the outer membrane of Gram-negative bacteria. They consist of a hydrophilic polysaccharide called the O-antigen, a core oligosaccharide, and a lipid portion known as Lipid A. The Lipid A component is responsible for the endotoxic activity of LPS, which can trigger a powerful immune response in animals, including humans. This response can lead to symptoms such as fever, inflammation, and septic shock, especially when large amounts of LPS are introduced into the bloodstream.

Interleukin-8 (IL-8) receptors are a type of G protein-coupled receptor that bind to and are activated by the cytokine IL-8. There are two main types of IL-8 receptors, known as CXCR1 and CXCR2.

IL-8B, also known as CXCR2, is a gene that encodes for the Interleukin-8 receptor B. This receptor is found on the surface of various cells, including neutrophils, monocytes, and endothelial cells. It plays a crucial role in the immune response, particularly in the recruitment and activation of neutrophils to sites of infection or inflammation.

IL-8B has a high affinity for IL-8 and other related chemokines, such as CXCL1, CXCL5, and CXCL7. Upon binding to its ligand, IL-8B activates various signaling pathways that lead to the mobilization and migration of neutrophils towards the site of inflammation. This process is critical for the elimination of invading pathogens and the resolution of inflammation.

However, excessive or prolonged activation of IL-8B has been implicated in various pathological conditions, including chronic inflammation, cancer, and autoimmune diseases. Therefore, targeting IL-8B with therapeutic agents has emerged as a promising strategy for the treatment of these conditions.

Cytoplasmic granules are small, membrane-bound organelles or inclusions found within the cytoplasm of cells. They contain various substances such as proteins, lipids, carbohydrates, and genetic material. Cytoplasmic granules have diverse functions depending on their specific composition and cellular location. Some examples include:

1. Secretory granules: These are found in secretory cells and store hormones, neurotransmitters, or enzymes before they are released by exocytosis.
2. Lysosomes: These are membrane-bound organelles that contain hydrolytic enzymes for intracellular digestion of waste materials, foreign substances, and damaged organelles.
3. Melanosomes: Found in melanocytes, these granules produce and store the pigment melanin, which is responsible for skin, hair, and eye color.
4. Weibel-Palade bodies: These are found in endothelial cells and store von Willebrand factor and P-selectin, which play roles in hemostasis and inflammation.
5. Peroxisomes: These are single-membrane organelles that contain enzymes for various metabolic processes, such as β-oxidation of fatty acids and detoxification of harmful substances.
6. Lipid bodies (also called lipid droplets): These are cytoplasmic granules that store neutral lipids, such as triglycerides and cholesteryl esters. They play a role in energy metabolism and intracellular signaling.
7. Glycogen granules: These are cytoplasmic inclusions that store glycogen, a polysaccharide used for energy storage in animals.
8. Protein bodies: Found in plants, these granules store excess proteins and help regulate protein homeostasis within the cell.
9. Electron-dense granules: These are found in certain immune cells, such as mast cells and basophils, and release mediators like histamine during an allergic response.
10. Granules of unknown composition or function may also be present in various cell types.

Platelet-activating factor (PAF) is a potent phospholipid mediator that plays a significant role in various inflammatory and immune responses. It is a powerful lipid signaling molecule released mainly by activated platelets, neutrophils, monocytes, endothelial cells, and other cell types during inflammation or injury.

PAF has a molecular structure consisting of an alkyl chain linked to a glycerol moiety, a phosphate group, and an sn-2 acetyl group. This unique structure allows PAF to bind to its specific G protein-coupled receptor (PAF-R) on the surface of target cells, triggering various intracellular signaling cascades that result in cell activation, degranulation, and aggregation.

The primary functions of PAF include:

1. Platelet activation and aggregation: PAF stimulates platelets to aggregate, release their granules, and activate the coagulation cascade, which can lead to thrombus formation.
2. Neutrophil and monocyte activation: PAF activates these immune cells, leading to increased adhesion, degranulation, and production of reactive oxygen species (ROS) and pro-inflammatory cytokines.
3. Vasodilation and increased vascular permeability: PAF can cause vasodilation by acting on endothelial cells, leading to an increase in blood flow and facilitating the extravasation of immune cells into inflamed tissues.
4. Bronchoconstriction: In the respiratory system, PAF can induce bronchoconstriction and recruitment of inflammatory cells, contributing to asthma symptoms.
5. Neurotransmission modulation: PAF has been implicated in neuroinflammation and may play a role in neuronal excitability, synaptic plasticity, and cognitive functions.

Dysregulated PAF signaling has been associated with several pathological conditions, including atherosclerosis, sepsis, acute respiratory distress syndrome (ARDS), ischemia-reperfusion injury, and neuroinflammatory disorders. Therefore, targeting the PAF pathway may provide therapeutic benefits in these diseases.

NADPH oxidase is an enzyme complex that plays a crucial role in the production of reactive oxygen species (ROS) in various cell types. The primary function of NADPH oxidase is to catalyze the transfer of electrons from NADPH to molecular oxygen, resulting in the formation of superoxide radicals. This enzyme complex consists of several subunits, including two membrane-bound components (gp91phox and p22phox) and several cytosolic components (p47phox, p67phox, p40phox, and rac1 or rac2). Upon activation, these subunits assemble to form a functional enzyme complex that generates ROS, which serve as important signaling molecules in various cellular processes. However, excessive or uncontrolled production of ROS by NADPH oxidase has been implicated in the pathogenesis of several diseases, such as cardiovascular disorders, neurodegenerative diseases, and cancer.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Cell-derived microparticles (CDMs), also known as microvesicles or microparticles, are small membrane-bound particles that are released from the cell surface upon activation or apoptosis of various cell types, including platelets, leukocytes, endothelial cells, and red blood cells. CDMs range in size from 0.1 to 1.0 micrometers in diameter and contain a variety of bioactive molecules, such as lipids, proteins, and nucleic acids, which can be transferred to neighboring or distant cells, thereby modulating their function.

CDMs have been implicated in various physiological and pathological processes, including coagulation, inflammation, immune response, angiogenesis, and cancer progression. They have also emerged as potential biomarkers for various diseases, such as cardiovascular disease, sepsis, and cancer, due to their distinct molecular signature and abundance in body fluids, such as blood, urine, and cerebrospinal fluid.

The mechanisms of CDM formation and release are complex and involve several cellular processes, including cytoskeletal rearrangement, membrane budding, and vesicle shedding. The molecular composition of CDMs reflects their cellular origin and activation state, and can be analyzed by various techniques, such as flow cytometry, proteomics, and transcriptomics, to gain insights into their biological functions and clinical relevance.

Reperfusion injury is a complex pathophysiological process that occurs when blood flow is restored to previously ischemic tissues, leading to further tissue damage. This phenomenon can occur in various clinical settings such as myocardial infarction (heart attack), stroke, or peripheral artery disease after an intervention aimed at restoring perfusion.

The restoration of blood flow leads to the generation of reactive oxygen species (ROS) and inflammatory mediators, which can cause oxidative stress, cellular damage, and activation of the immune system. This results in a cascade of events that may lead to microvascular dysfunction, capillary leakage, and tissue edema, further exacerbating the injury.

Reperfusion injury is an important consideration in the management of ischemic events, as interventions aimed at restoring blood flow must be carefully balanced with potential harm from reperfusion injury. Strategies to mitigate reperfusion injury include ischemic preconditioning (exposing the tissue to short periods of ischemia before a prolonged ischemic event), ischemic postconditioning (applying brief periods of ischemia and reperfusion after restoring blood flow), remote ischemic preconditioning (ischemia applied to a distant organ or tissue to protect the target organ), and pharmacological interventions that scavenge ROS, reduce inflammation, or improve microvascular function.

Tumor Necrosis Factor-alpha (TNF-α) is a cytokine, a type of small signaling protein involved in immune response and inflammation. It is primarily produced by activated macrophages, although other cell types such as T-cells, natural killer cells, and mast cells can also produce it.

TNF-α plays a crucial role in the body's defense against infection and tissue injury by mediating inflammatory responses, activating immune cells, and inducing apoptosis (programmed cell death) in certain types of cells. It does this by binding to its receptors, TNFR1 and TNFR2, which are found on the surface of many cell types.

In addition to its role in the immune response, TNF-α has been implicated in the pathogenesis of several diseases, including autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as cancer, where it can promote tumor growth and metastasis.

Therapeutic agents that target TNF-α, such as infliximab, adalimumab, and etanercept, have been developed to treat these conditions. However, these drugs can also increase the risk of infections and other side effects, so their use must be carefully monitored.

Traumatic shock is a type of physiological response that occurs when an individual experiences a severe physical trauma, such as severe injury, burns, or bleeding. This condition is characterized by inadequate tissue perfusion and oxygenation, which can lead to cellular damage and organ dysfunction. The primary cause of traumatic shock is a significant decrease in blood volume due to hemorrhage, which reduces the amount of oxygen and nutrients delivered to tissues and organs.

The symptoms of traumatic shock include:

1. Hypotension (low blood pressure)
2. Tachycardia (rapid heart rate)
3. Altered mental status (confusion, agitation, or lethargy)
4. Cool, clammy skin
5. Weak or absent peripheral pulses
6. Rapid, shallow breathing
7. Decreased urine output
8. Lactic acidosis (elevated levels of lactic acid in the blood)
9. Metabolic disturbances

Traumatic shock is a medical emergency that requires immediate treatment to prevent further tissue damage and organ dysfunction. Treatment typically involves fluid resuscitation, blood transfusion, and surgery to control bleeding. In some cases, medications such as vasopressors may be necessary to maintain blood pressure and perfusion to vital organs.

Flow cytometry is a medical and research technique used to measure physical and chemical characteristics of cells or particles, one cell at a time, as they flow in a fluid stream through a beam of light. The properties measured include:

* Cell size (light scatter)
* Cell internal complexity (granularity, also light scatter)
* Presence or absence of specific proteins or other molecules on the cell surface or inside the cell (using fluorescent antibodies or other fluorescent probes)

The technique is widely used in cell counting, cell sorting, protein engineering, biomarker discovery and monitoring disease progression, particularly in hematology, immunology, and cancer research.

Decompression, in the medical context, refers to the process of reducing pressure on a body part or on a tissue, organ, or fluid within the body. This is often used to describe procedures that are intended to relieve excessive pressure built up inside the body, such as:

1. Decompression sickness treatment: Also known as "the bends," this condition occurs when nitrogen bubbles form in the blood and tissues due to rapid decompression, typically during scuba diving. Decompression involves using a hyperbaric chamber to slowly reduce the pressure and allow the nitrogen to safely dissolve and be eliminated from the body.

2. Spinal decompression: This is a minimally invasive therapeutic treatment for managing pain in the spine, often used to alleviate pressure on nerves or discs within the spinal column. Decompression can be achieved through various methods, such as traction, motorized tables, or vacuum-created devices that gently stretch and realign the spine, promoting circulation and reducing pressure on compressed nerves.

3. Ear decompression: This procedure is used to equalize pressure in the middle ear during scuba diving or flying at high altitudes. It can be achieved by swallowing, yawning, or performing the Valsalva maneuver (pinching the nose and blowing gently). In some cases, a doctor may need to perform a myringotomy, which involves making a small incision in the eardrum to relieve pressure.

4. Decompression of body parts: This can be relevant in situations where a part of the body is subjected to increased pressure due to various reasons, such as compartment syndrome or edema. In these cases, decompression may involve surgical intervention to release the pressure and prevent further damage to tissues and nerves.

Please note that this list is not exhaustive, and there might be other medical scenarios where the term "decompression" is used in a similar context.

CD11 is a group of integrin proteins that are present on the surface of various immune cells, including neutrophils, monocytes, and macrophages. They play a crucial role in the adhesion and migration of these cells to sites of inflammation or injury. CD11 includes three distinct subunits: CD11a (also known as LFA-1), CD11b (also known as Mac-1 or Mo1), and CD11c (also known as p150,95).

Antigens are substances that can stimulate an immune response in the body. In the context of CD11, antigens may refer to specific molecules or structures on pathogens such as bacteria or viruses that can be recognized by CD11-expressing immune cells. These antigens bind to CD11 and trigger a series of intracellular signaling events that lead to the activation and migration of the immune cells to the site of infection or injury.

Therefore, the medical definition of 'antigens, CD11' may refer to specific molecules or structures on pathogens that can bind to CD11 proteins on immune cells and trigger an immune response.

A lung is a pair of spongy, elastic organs in the chest that work together to enable breathing. They are responsible for taking in oxygen and expelling carbon dioxide through the process of respiration. The left lung has two lobes, while the right lung has three lobes. The lungs are protected by the ribcage and are covered by a double-layered membrane called the pleura. The trachea divides into two bronchi, which further divide into smaller bronchioles, leading to millions of tiny air sacs called alveoli, where the exchange of gases occurs.

Selectins are a type of cell adhesion molecule that play a crucial role in the inflammatory response. They are involved in the initial attachment and rolling of white blood cells (such as neutrophils) along the walls of blood vessels, which is an essential step in the extravasation process that allows these cells to migrate from the bloodstream into surrounding tissues in order to respond to infection or injury.

There are three main types of selectins: E-selectin (expressed on endothelial cells), P-selectin (expressed on both endothelial cells and platelets), and L-selectin (expressed on leukocytes). These proteins recognize specific carbohydrate structures on the surface of white blood cells, allowing them to bind together and initiate the inflammatory cascade. Selectins have been implicated in various inflammatory diseases, including atherosclerosis, asthma, and rheumatoid arthritis, making them potential targets for therapeutic intervention.

Reactive Oxygen Species (ROS) are highly reactive molecules containing oxygen, including peroxides, superoxide, hydroxyl radical, and singlet oxygen. They are naturally produced as byproducts of normal cellular metabolism in the mitochondria, and can also be generated by external sources such as ionizing radiation, tobacco smoke, and air pollutants. At low or moderate concentrations, ROS play important roles in cell signaling and homeostasis, but at high concentrations, they can cause significant damage to cell structures, including lipids, proteins, and DNA, leading to oxidative stress and potential cell death.

Wegener Granulomatosis is a rare, chronic granulomatous vasculitis that affects small and medium-sized blood vessels. It is also known as granulomatosis with polyangiitis (GPA). The disease primarily involves the respiratory tract (nose, sinuses, trachea, and lungs) and kidneys but can affect other organs as well.

The characteristic features of Wegener Granulomatosis include necrotizing granulomas, vasculitis, and inflammation of the blood vessel walls. These abnormalities can lead to various symptoms such as cough, shortness of breath, nosebleeds, sinus congestion, skin lesions, joint pain, and kidney problems.

The exact cause of Wegener Granulomatosis is unknown, but it is believed to be an autoimmune disorder where the body's immune system mistakenly attacks its own tissues and organs. The diagnosis of Wegener Granulomatosis typically involves a combination of clinical symptoms, laboratory tests, imaging studies, and biopsy findings. Treatment usually includes immunosuppressive therapy to control the inflammation and prevent further damage to the affected organs.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Vasculitis is a group of disorders characterized by inflammation of the blood vessels, which can cause changes in the vessel walls including thickening, narrowing, or weakening. These changes can restrict blood flow, leading to organ and tissue damage. The specific symptoms and severity of vasculitis depend on the size and location of the affected blood vessels and the extent of inflammation. Vasculitis can affect any organ system in the body, and its causes can vary, including infections, autoimmune disorders, or exposure to certain medications or chemicals.

Complement C5 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. The complement system is a complex series of biochemical reactions that help to identify and destroy foreign substances, such as bacteria and viruses.

Complement C5 is one of several proteins in the complement system that are activated in a cascading manner in response to an activating event, such as the binding of an antibody to a pathogen. Once activated, Complement C5 can be cleaved into two smaller proteins, C5a and C5b.

C5a is a powerful anaphylatoxin, which means it can cause the release of histamine from mast cells and basophils, leading to inflammation and increased vascular permeability. It also acts as a chemoattractant, drawing immune cells to the site of infection or injury.

C5b, on the other hand, plays a role in the formation of the membrane attack complex (MAC), which is a protein structure that can punch holes in the membranes of pathogens, leading to their lysis and destruction.

Overall, Complement C5 is an important component of the immune system's response to infection and injury, helping to eliminate pathogens and damaged cells from the body.

GPI-linked proteins are a type of cell surface protein that are attached to the plasma membrane via a glycosylphosphatidylinositol (GPI) anchor. The GPI anchor is a complex glycolipid molecule that acts as a molecular tether, connecting the protein to the outer leaflet of the lipid bilayer of the cell membrane.

The GPI anchor is synthesized in the endoplasmic reticulum (ER) and added to proteins in the ER or Golgi apparatus during protein trafficking. The addition of the GPI anchor to a protein occurs in a post-translational modification process called GPI anchoring, which involves the transfer of the GPI moiety from a lipid carrier to the carboxyl terminus of the protein.

GPI-linked proteins are found on the surface of many different types of cells, including red blood cells, immune cells, and nerve cells. They play important roles in various cellular processes, such as cell signaling, cell adhesion, and enzyme function. Some GPI-linked proteins also serve as receptors for bacterial toxins and viruses, making them potential targets for therapeutic intervention.

Cytokines are a broad and diverse category of small signaling proteins that are secreted by various cells, including immune cells, in response to different stimuli. They play crucial roles in regulating the immune response, inflammation, hematopoiesis, and cellular communication.

Cytokines mediate their effects by binding to specific receptors on the surface of target cells, which triggers intracellular signaling pathways that ultimately result in changes in gene expression, cell behavior, and function. Some key functions of cytokines include:

1. Regulating the activation, differentiation, and proliferation of immune cells such as T cells, B cells, natural killer (NK) cells, and macrophages.
2. Coordinating the inflammatory response by recruiting immune cells to sites of infection or tissue damage and modulating their effector functions.
3. Regulating hematopoiesis, the process of blood cell formation in the bone marrow, by controlling the proliferation, differentiation, and survival of hematopoietic stem and progenitor cells.
4. Modulating the development and function of the nervous system, including neuroinflammation, neuroprotection, and neuroregeneration.

Cytokines can be classified into several categories based on their structure, function, or cellular origin. Some common types of cytokines include interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs), chemokines, colony-stimulating factors (CSFs), and transforming growth factors (TGFs). Dysregulation of cytokine production and signaling has been implicated in various pathological conditions, such as autoimmune diseases, chronic inflammation, cancer, and neurodegenerative disorders.

Calgranulin A is also known as S100A8 or MRP-14. It is a calcium-binding protein that belongs to the S100 family of proteins. Calgranulin A is primarily found in the cytoplasm of neutrophils, a type of white blood cell involved in inflammation and immune response.

Calgranulin A can be released from neutrophils during inflammation and has been implicated in various biological processes, including regulation of innate immunity, inflammation, and cancer progression. It can also interact with other proteins to form heterodimers or multimers, such as calprotectin (S100A8/S100A9), which has been associated with several pathological conditions, including autoimmune diseases, infections, and cancer.

In medical research, Calgranulin A is often used as a biomarker for various inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, and chronic obstructive pulmonary disease (COPD). Elevated levels of Calgranulin A in body fluids, such as blood or sputum, may indicate the presence of an ongoing inflammatory response.

Calcimycin is a ionophore compound that is produced by the bacterium Streptomyces chartreusensis. It is also known as Calcineurin A inhibitor because it can bind to and inhibit the activity of calcineurin, a protein phosphatase. In medical research, calcimycin is often used to study calcium signaling in cells.
It has been also used in laboratory studies for its antiproliferative and pro-apoptotic effects on certain types of cancer cells. However, it is not approved for use as a drug in humans.

Bronchoalveolar lavage (BAL) fluid is a type of clinical specimen obtained through a procedure called bronchoalveolar lavage. This procedure involves inserting a bronchoscope into the lungs and instilling a small amount of saline solution into a specific area of the lung, then gently aspirating the fluid back out. The fluid that is recovered is called bronchoalveolar lavage fluid.

BAL fluid contains cells and other substances that are present in the lower respiratory tract, including the alveoli (the tiny air sacs where gas exchange occurs). By analyzing BAL fluid, doctors can diagnose various lung conditions, such as pneumonia, interstitial lung disease, and lung cancer. They can also monitor the effectiveness of treatments for these conditions by comparing the composition of BAL fluid before and after treatment.

BAL fluid is typically analyzed for its cellular content, including the number and type of white blood cells present, as well as for the presence of bacteria, viruses, or other microorganisms. The fluid may also be tested for various proteins, enzymes, and other biomarkers that can provide additional information about lung health and disease.

Complement C3a is a protein fragment that is generated during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by marking them for destruction and attracting immune cells to the site of infection or injury.

C3a is produced when the third component of the complement system (C3) is cleaved into two smaller fragments, C3a and C3b, during the complement activation cascade. C3a is a potent anaphylatoxin, which means it can cause the release of histamine and other mediators from mast cells and basophils, leading to inflammation, increased vascular permeability, and smooth muscle contraction.

C3a also has chemotactic properties, meaning it can attract immune cells such as neutrophils and monocytes to the site of complement activation. Additionally, C3a can modulate the activity of various immune cells, including dendritic cells, T cells, and B cells, and play a role in the regulation of the adaptive immune response.

It's important to note that while C3a has important functions in the immune response, uncontrolled or excessive activation of the complement system can lead to tissue damage and inflammation, contributing to the pathogenesis of various diseases such as autoimmune disorders, inflammatory diseases, and allergies.

P-Selectin is a type of cell adhesion molecule, specifically a member of the selectin family, that is involved in the inflammatory response. It is primarily expressed on the surface of activated platelets and endothelial cells. P-Selectin plays a crucial role in the initial interaction between leukocytes (white blood cells) and the vascular endothelium, which is an essential step in the recruitment of leukocytes to sites of inflammation or injury. This process helps to mediate the rolling and adhesion of leukocytes to the endothelial surface, facilitating their extravasation into the surrounding tissue. P-Selectin's function is regulated by its interaction with specific ligands on the surface of leukocytes, such as PSGL-1 (P-Selectin Glycoprotein Ligand-1).

Cell adhesion molecules (CAMs) are a type of protein found on the surface of cells that mediate the attachment or adhesion of cells to either other cells or to the extracellular matrix (ECM), which is the network of proteins and carbohydrates that provides structural and biochemical support to surrounding cells.

CAMs play crucial roles in various biological processes, including tissue development, differentiation, repair, and maintenance of tissue architecture and function. They are also involved in cell signaling, migration, and regulation of the immune response.

There are several types of CAMs, classified based on their structure and function, such as immunoglobulin-like CAMs (IgCAMs), cadherins, integrins, and selectins. Dysregulation of CAMs has been implicated in various diseases, including cancer, inflammation, and neurological disorders.

Leukocytes, also known as white blood cells (WBCs), are a crucial component of the human immune system. They are responsible for protecting the body against infections and foreign substances. Leukocytes are produced in the bone marrow and circulate throughout the body in the bloodstream and lymphatic system.

There are several types of leukocytes, including:

1. Neutrophils - These are the most abundant type of leukocyte and are primarily responsible for fighting bacterial infections. They contain enzymes that can destroy bacteria.
2. Lymphocytes - These are responsible for producing antibodies and destroying virus-infected cells, as well as cancer cells. There are two main types of lymphocytes: B-lymphocytes and T-lymphocytes.
3. Monocytes - These are the largest type of leukocyte and help to break down and remove dead or damaged tissues, as well as microorganisms.
4. Eosinophils - These play a role in fighting parasitic infections and are also involved in allergic reactions and inflammation.
5. Basophils - These release histamine and other chemicals that cause inflammation in response to allergens or irritants.

An abnormal increase or decrease in the number of leukocytes can indicate an underlying medical condition, such as an infection, inflammation, or a blood disorder.

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Acute Lung Injury (ALI) is a medical condition characterized by inflammation and damage to the lung tissue, which can lead to difficulty breathing and respiratory failure. It is often caused by direct or indirect injury to the lungs, such as pneumonia, sepsis, trauma, or inhalation of harmful substances.

The symptoms of ALI include shortness of breath, rapid breathing, cough, and low oxygen levels in the blood. The condition can progress rapidly and may require mechanical ventilation to support breathing. Treatment typically involves addressing the underlying cause of the injury, providing supportive care, and managing symptoms.

In severe cases, ALI can lead to Acute Respiratory Distress Syndrome (ARDS), a more serious and life-threatening condition that requires intensive care unit (ICU) treatment.

Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) is a type of cytokine, which is a small signaling protein involved in immune response and hematopoiesis (the formation of blood cells). GM-CSF's specific role is to stimulate the production, proliferation, and activation of granulocytes (a type of white blood cell that fights against infection) and macrophages (large white blood cells that eat foreign substances, bacteria, and dead or dying cells).

In medical terms, GM-CSF is often used in therapeutic settings to boost the production of white blood cells in patients undergoing chemotherapy or radiation treatment for cancer. This can help to reduce the risk of infection during these treatments. It can also be used to promote the growth and differentiation of stem cells in bone marrow transplant procedures.

NADH, NADPH oxidoreductases are a class of enzymes that catalyze the redox reaction between NADH or NADPH and various electron acceptors. These enzymes play a crucial role in cellular metabolism by transferring electrons from NADH or NADPH to other molecules, which is essential for many biochemical reactions.

NADH (nicotinamide adenine dinucleotide hydrogen) and NADPH (nicotinamide adenine dinucleotide phosphate hydrogen) are coenzymes that act as electron carriers in redox reactions. They consist of a nicotinamide ring, which undergoes reduction or oxidation by accepting or donating electrons and a proton (H+).

NADH, NADPH oxidoreductases are classified based on their structure and mechanism of action. Some examples include:

1. Dehydrogenases: These enzymes catalyze the oxidation of NADH or NADPH to NAD+ or NADP+ while reducing an organic substrate. Examples include lactate dehydrogenase, alcohol dehydrogenase, and malate dehydrogenase.
2. Oxidases: These enzymes catalyze the oxidation of NADH or NADPH to NAD+ or NADP+ while reducing molecular oxygen (O2) to water (H2O). Examples include NADH oxidase and NADPH oxidase.
3. Reductases: These enzymes catalyze the reduction of various electron acceptors using NADH or NADPH as a source of electrons. Examples include glutathione reductase, thioredoxin reductase, and nitrate reductase.

Overall, NADH, NADPH oxidoreductases are essential for maintaining the redox balance in cells and play a critical role in various metabolic pathways, including energy production, detoxification, and biosynthesis.

Cell movement, also known as cell motility, refers to the ability of cells to move independently and change their location within tissue or inside the body. This process is essential for various biological functions, including embryonic development, wound healing, immune responses, and cancer metastasis.

There are several types of cell movement, including:

1. **Crawling or mesenchymal migration:** Cells move by extending and retracting protrusions called pseudopodia or filopodia, which contain actin filaments. This type of movement is common in fibroblasts, immune cells, and cancer cells during tissue invasion and metastasis.
2. **Amoeboid migration:** Cells move by changing their shape and squeezing through tight spaces without forming protrusions. This type of movement is often observed in white blood cells (leukocytes) as they migrate through the body to fight infections.
3. **Pseudopodial extension:** Cells extend pseudopodia, which are temporary cytoplasmic projections containing actin filaments. These protrusions help the cell explore its environment and move forward.
4. **Bacterial flagellar motion:** Bacteria use a whip-like structure called a flagellum to propel themselves through their environment. The rotation of the flagellum is driven by a molecular motor in the bacterial cell membrane.
5. **Ciliary and ependymal movement:** Ciliated cells, such as those lining the respiratory tract and fallopian tubes, have hair-like structures called cilia that beat in coordinated waves to move fluids or mucus across the cell surface.

Cell movement is regulated by a complex interplay of signaling pathways, cytoskeletal rearrangements, and adhesion molecules, which enable cells to respond to environmental cues and navigate through tissues.

An antigen-antibody complex is a type of immune complex that forms when an antibody binds to a specific antigen. An antigen is any substance that triggers an immune response, while an antibody is a protein produced by the immune system to neutralize or destroy foreign substances like antigens.

When an antibody binds to an antigen, it forms a complex that can be either soluble or insoluble. Soluble complexes are formed when the antigen is small and can move freely through the bloodstream. Insoluble complexes, on the other hand, are formed when the antigen is too large to move freely, such as when it is part of a bacterium or virus.

The formation of antigen-antibody complexes plays an important role in the immune response. Once formed, these complexes can be recognized and cleared by other components of the immune system, such as phagocytes, which help to prevent further damage to the body. However, in some cases, the formation of large numbers of antigen-antibody complexes can lead to inflammation and tissue damage, contributing to the development of certain autoimmune diseases.

Hemorrhagic shock is a type of shock that occurs when there is significant blood loss leading to inadequate perfusion of tissues and organs. It is characterized by hypovolemia (low blood volume), hypotension (low blood pressure), tachycardia (rapid heart rate), and decreased urine output. Hemorrhagic shock can be classified into four stages based on the amount of blood loss and hemodynamic changes. In severe cases, it can lead to multi-organ dysfunction and death if not treated promptly and effectively.

HL-60 cells are a type of human promyelocytic leukemia cell line that is commonly used in scientific research. They are named after the hospital where they were first isolated, the Hospital of the University of Pennsylvania (HUP) and the 60th culture attempt to grow these cells.

HL-60 cells have the ability to differentiate into various types of blood cells, such as granulocytes, monocytes, and macrophages, when exposed to certain chemical compounds or under specific culturing conditions. This makes them a valuable tool for studying the mechanisms of cell differentiation, proliferation, and apoptosis (programmed cell death).

HL-60 cells are also often used in toxicity studies, drug discovery and development, and research on cancer, inflammation, and infectious diseases. They can be easily grown in the lab and have a stable genotype, making them ideal for use in standardized experiments and comparisons between different studies.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Uric acid is a chemical compound that is formed when the body breaks down purines, which are substances that are found naturally in certain foods such as steak, organ meats and seafood, as well as in our own cells. After purines are broken down, they turn into uric acid and then get excreted from the body in the urine.

However, if there is too much uric acid in the body, it can lead to a condition called hyperuricemia. High levels of uric acid can cause gout, which is a type of arthritis that causes painful swelling and inflammation in the joints, especially in the big toe. Uric acid can also form crystals that can collect in the kidneys and lead to kidney stones.

It's important for individuals with gout or recurrent kidney stones to monitor their uric acid levels and follow a treatment plan prescribed by their healthcare provider, which may include medications to lower uric acid levels and dietary modifications.

Cell aggregation is the process by which individual cells come together and adhere to each other to form a group or cluster. This phenomenon can occur naturally during embryonic development, tissue repair, and wound healing, as well as in the formation of multicellular organisms such as slime molds. In some cases, cell aggregation may also be induced in the laboratory setting through the use of various techniques, including the use of cell culture surfaces that promote cell-to-cell adhesion or the addition of factors that stimulate the expression of adhesion molecules on the cell surface.

Cell aggregation can be influenced by a variety of factors, including the type and properties of the cells involved, as well as environmental conditions such as pH, temperature, and nutrient availability. The ability of cells to aggregate is often mediated by the presence of adhesion molecules on the cell surface, such as cadherins, integrins, and immunoglobulin-like cell adhesion molecules (Ig-CAMs). These molecules interact with each other and with extracellular matrix components to promote cell-to-cell adhesion and maintain the stability of the aggregate.

In some contexts, abnormal or excessive cell aggregation can contribute to the development of diseases such as cancer, fibrosis, and inflammatory disorders. For example, the aggregation of cancer cells can facilitate their invasion and metastasis, while the accumulation of fibrotic cells in tissues can lead to organ dysfunction and failure. Understanding the mechanisms that regulate cell aggregation is therefore an important area of research with potential implications for the development of new therapies and treatments for a variety of diseases.

Alpha 1-antitrypsin (AAT, or α1-antiproteinase, A1AP) is a protein that is primarily produced by the liver and released into the bloodstream. It belongs to a group of proteins called serine protease inhibitors, which help regulate inflammation and protect tissues from damage caused by enzymes involved in the immune response.

Alpha 1-antitrypsin is particularly important for protecting the lungs from damage caused by neutrophil elastase, an enzyme released by white blood cells called neutrophils during inflammation. In the lungs, AAT binds to and inhibits neutrophil elastase, preventing it from degrading the extracellular matrix and damaging lung tissue.

Deficiency in alpha 1-antitrypsin can lead to chronic obstructive pulmonary disease (COPD) and liver disease. The most common cause of AAT deficiency is a genetic mutation that results in abnormal folding and accumulation of the protein within liver cells, leading to reduced levels of functional AAT in the bloodstream. This condition is called alpha 1-antitrypsin deficiency (AATD) and can be inherited in an autosomal codominant manner. Individuals with severe AATD may require augmentation therapy with intravenous infusions of purified human AAT to help prevent lung damage.

Chemokines are a family of small cytokines, or signaling proteins, that are secreted by cells and play an important role in the immune system. They are chemotactic, meaning they can attract and guide the movement of various immune cells to specific locations within the body. Chemokines do this by binding to G protein-coupled receptors on the surface of target cells, initiating a signaling cascade that leads to cell migration.

There are four main subfamilies of chemokines, classified based on the arrangement of conserved cysteine residues near the amino terminus: CXC, CC, C, and CX3C. Different chemokines have specific roles in inflammation, immune surveillance, hematopoiesis, and development. Dysregulation of chemokine function has been implicated in various diseases, including autoimmune disorders, infections, and cancer.

In summary, Chemokines are a group of signaling proteins that play a crucial role in the immune system by directing the movement of immune cells to specific locations within the body, thus helping to coordinate the immune response.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Enzyme activation refers to the process by which an enzyme becomes biologically active and capable of carrying out its specific chemical or biological reaction. This is often achieved through various post-translational modifications, such as proteolytic cleavage, phosphorylation, or addition of cofactors or prosthetic groups to the enzyme molecule. These modifications can change the conformation or structure of the enzyme, exposing or creating a binding site for the substrate and allowing the enzymatic reaction to occur.

For example, in the case of proteolytic cleavage, an inactive precursor enzyme, known as a zymogen, is cleaved into its active form by a specific protease. This is seen in enzymes such as trypsin and chymotrypsin, which are initially produced in the pancreas as inactive precursors called trypsinogen and chymotrypsinogen, respectively. Once they reach the small intestine, they are activated by enteropeptidase, a protease that cleaves a specific peptide bond, releasing the active enzyme.

Phosphorylation is another common mechanism of enzyme activation, where a phosphate group is added to a specific serine, threonine, or tyrosine residue on the enzyme by a protein kinase. This modification can alter the conformation of the enzyme and create a binding site for the substrate, allowing the enzymatic reaction to occur.

Enzyme activation is a crucial process in many biological pathways, as it allows for precise control over when and where specific reactions take place. It also provides a mechanism for regulating enzyme activity in response to various signals and stimuli, such as hormones, neurotransmitters, or changes in the intracellular environment.

A cell membrane, also known as the plasma membrane, is a thin semi-permeable phospholipid bilayer that surrounds all cells in animals, plants, and microorganisms. It functions as a barrier to control the movement of substances in and out of the cell, allowing necessary molecules such as nutrients, oxygen, and signaling molecules to enter while keeping out harmful substances and waste products. The cell membrane is composed mainly of phospholipids, which have hydrophilic (water-loving) heads and hydrophobic (water-fearing) tails. This unique structure allows the membrane to be flexible and fluid, yet selectively permeable. Additionally, various proteins are embedded in the membrane that serve as channels, pumps, receptors, and enzymes, contributing to the cell's overall functionality and communication with its environment.

CD (cluster of differentiation) antigens are cell-surface proteins that are expressed on leukocytes (white blood cells) and can be used to identify and distinguish different subsets of these cells. They are important markers in the field of immunology and hematology, and are commonly used to diagnose and monitor various diseases, including cancer, autoimmune disorders, and infectious diseases.

CD antigens are designated by numbers, such as CD4, CD8, CD19, etc., which refer to specific proteins found on the surface of different types of leukocytes. For example, CD4 is a protein found on the surface of helper T cells, while CD8 is found on cytotoxic T cells.

CD antigens can be used as targets for immunotherapy, such as monoclonal antibody therapy, in which antibodies are designed to bind to specific CD antigens and trigger an immune response against cancer cells or infected cells. They can also be used as markers to monitor the effectiveness of treatments and to detect minimal residual disease (MRD) after treatment.

It's important to note that not all CD antigens are exclusive to leukocytes, some can be found on other cell types as well, and their expression can vary depending on the activation state or differentiation stage of the cells.

Exocytosis is the process by which cells release molecules, such as hormones or neurotransmitters, to the extracellular space. This process involves the transport of these molecules inside vesicles (membrane-bound sacs) to the cell membrane, where they fuse and release their contents to the outside of the cell. It is a crucial mechanism for intercellular communication and the regulation of various physiological processes in the body.

Chemokines are a family of small signaling proteins that are involved in immune regulation and inflammation. They mediate their effects by interacting with specific cell surface receptors, leading to the activation and migration of various types of immune cells. Chemokines can be divided into four subfamilies based on the arrangement of conserved cysteine residues near the N-terminus: CXC, CC, C, and CX3C.

CXC chemokines are characterized by the presence of a single amino acid (X) between the first two conserved cysteine residues. They play important roles in the recruitment and activation of neutrophils, which are critical effector cells in the early stages of inflammation. CXC chemokines can be further divided into two subgroups based on the presence or absence of a specific amino acid sequence (ELR motif) near the N-terminus: ELR+ and ELR-.

ELR+ CXC chemokines, such as IL-8, are potent chemoattractants for neutrophils and play important roles in the recruitment of these cells to sites of infection or injury. They bind to and activate the CXCR1 and CXCR2 receptors on the surface of neutrophils, leading to their migration towards the source of the chemokine.

ELR- CXC chemokines, such as IP-10 and MIG, are involved in the recruitment of T cells and other immune cells to sites of inflammation. They bind to and activate different receptors, such as CXCR3, on the surface of these cells, leading to their migration towards the source of the chemokine.

Overall, CXC chemokines play important roles in the regulation of immune responses and inflammation, and dysregulation of their expression or activity has been implicated in a variety of diseases, including cancer, autoimmune disorders, and infectious diseases.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Intercellular Adhesion Molecule-1 (ICAM-1), also known as CD54, is a transmembrane glycoprotein expressed on the surface of various cell types including endothelial cells, fibroblasts, and immune cells. ICAM-1 plays a crucial role in the inflammatory response and the immune system by mediating the adhesion of leukocytes (white blood cells) to the endothelium, allowing them to migrate into surrounding tissues during an immune response or inflammation.

ICAM-1 contains five immunoglobulin-like domains in its extracellular region and binds to several integrins present on leukocytes, such as LFA-1 (lymphocyte function-associated antigen 1) and Mac-1 (macrophage-1 antigen). This interaction facilitates the firm adhesion of leukocytes to the endothelium, which is a critical step in the extravasation process.

In addition to its role in inflammation and immunity, ICAM-1 has been implicated in several pathological conditions, including atherosclerosis, cancer, and autoimmune diseases. Increased expression of ICAM-1 on endothelial cells is associated with the recruitment of immune cells to sites of injury or infection, making it an important target for therapeutic interventions in various inflammatory disorders.

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Hydrogen peroxide (H2O2) is a colorless, odorless, clear liquid with a slightly sweet taste, although drinking it is harmful and can cause poisoning. It is a weak oxidizing agent and is used as an antiseptic and a bleaching agent. In diluted form, it is used to disinfect wounds and kill bacteria and viruses on the skin; in higher concentrations, it can be used to bleach hair or remove stains from clothing. It is also used as a propellant in rocketry and in certain industrial processes. Chemically, hydrogen peroxide is composed of two hydrogen atoms and two oxygen atoms, and it is structurally similar to water (H2O), with an extra oxygen atom. This gives it its oxidizing properties, as the additional oxygen can be released and used to react with other substances.

Immunologic receptors are specialized proteins found on the surface of immune cells that recognize and bind to specific molecules, known as antigens, on the surface of pathogens or infected cells. This binding triggers a series of intracellular signaling events that activate the immune cell and initiate an immune response.

There are several types of immunologic receptors, including:

1. T-cell receptors (TCRs): These receptors are found on the surface of T cells and recognize antigens presented in the context of major histocompatibility complex (MHC) molecules.
2. B-cell receptors (BCRs): These receptors are found on the surface of B cells and recognize free antigens in solution.
3. Pattern recognition receptors (PRRs): These receptors are found inside immune cells and recognize conserved molecular patterns associated with pathogens, such as lipopolysaccharides and flagellin.
4. Fc receptors: These receptors are found on the surface of various immune cells and bind to the constant region of antibodies, mediating effector functions such as phagocytosis and antibody-dependent cellular cytotoxicity (ADCC).

Immunologic receptors play a critical role in the recognition and elimination of pathogens and infected cells, and dysregulation of these receptors can lead to immune disorders and diseases.

Membrane glycoproteins are proteins that contain oligosaccharide chains (glycans) covalently attached to their polypeptide backbone. They are integral components of biological membranes, spanning the lipid bilayer and playing crucial roles in various cellular processes.

The glycosylation of these proteins occurs in the endoplasmic reticulum (ER) and Golgi apparatus during protein folding and trafficking. The attached glycans can vary in structure, length, and composition, which contributes to the diversity of membrane glycoproteins.

Membrane glycoproteins can be classified into two main types based on their orientation within the lipid bilayer:

1. Type I (N-linked): These glycoproteins have a single transmembrane domain and an extracellular N-terminus, where the oligosaccharides are predominantly attached via asparagine residues (Asn-X-Ser/Thr sequon).
2. Type II (C-linked): These glycoproteins possess two transmembrane domains and an intracellular C-terminus, with the oligosaccharides linked to tryptophan residues via a mannose moiety.

Membrane glycoproteins are involved in various cellular functions, such as:

* Cell adhesion and recognition
* Receptor-mediated signal transduction
* Enzymatic catalysis
* Transport of molecules across membranes
* Cell-cell communication
* Immunological responses

Some examples of membrane glycoproteins include cell surface receptors (e.g., growth factor receptors, cytokine receptors), adhesion molecules (e.g., integrins, cadherins), and transporters (e.g., ion channels, ABC transporters).

Up-regulation is a term used in molecular biology and medicine to describe an increase in the expression or activity of a gene, protein, or receptor in response to a stimulus. This can occur through various mechanisms such as increased transcription, translation, or reduced degradation of the molecule. Up-regulation can have important functional consequences, for example, enhancing the sensitivity or response of a cell to a hormone, neurotransmitter, or drug. It is a normal physiological process that can also be induced by disease or pharmacological interventions.

p38 Mitogen-Activated Protein Kinases (p38 MAPKs) are a family of conserved serine-threonine protein kinases that play crucial roles in various cellular processes, including inflammation, immune response, differentiation, apoptosis, and stress responses. They are activated by diverse stimuli such as cytokines, ultraviolet radiation, heat shock, osmotic stress, and lipopolysaccharides (LPS).

Once activated, p38 MAPKs phosphorylate and regulate several downstream targets, including transcription factors and other protein kinases. This regulation leads to the expression of genes involved in inflammation, cell cycle arrest, and apoptosis. Dysregulation of p38 MAPK signaling has been implicated in various diseases, such as cancer, neurodegenerative disorders, and autoimmune diseases. Therefore, p38 MAPKs are considered promising targets for developing new therapeutic strategies to treat these conditions.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Anti-inflammatory agents are a class of drugs or substances that reduce inflammation in the body. They work by inhibiting the production of inflammatory mediators, such as prostaglandins and leukotrienes, which are released during an immune response and contribute to symptoms like pain, swelling, redness, and warmth.

There are two main types of anti-inflammatory agents: steroidal and nonsteroidal. Steroidal anti-inflammatory drugs (SAIDs) include corticosteroids, which mimic the effects of hormones produced by the adrenal gland. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a larger group that includes both prescription and over-the-counter medications, such as aspirin, ibuprofen, naproxen, and celecoxib.

While both types of anti-inflammatory agents can be effective in reducing inflammation and relieving symptoms, they differ in their mechanisms of action, side effects, and potential risks. Long-term use of NSAIDs, for example, can increase the risk of gastrointestinal bleeding, kidney damage, and cardiovascular events. Corticosteroids can have significant side effects as well, particularly with long-term use, including weight gain, mood changes, and increased susceptibility to infections.

It's important to use anti-inflammatory agents only as directed by a healthcare provider, and to be aware of potential risks and interactions with other medications or health conditions.

Serine endopeptidases are a type of enzymes that cleave peptide bonds within proteins (endopeptidases) and utilize serine as the nucleophilic amino acid in their active site for catalysis. These enzymes play crucial roles in various biological processes, including digestion, blood coagulation, and programmed cell death (apoptosis). Examples of serine endopeptidases include trypsin, chymotrypsin, thrombin, and elastase.

Capillary permeability refers to the ability of substances to pass through the walls of capillaries, which are the smallest blood vessels in the body. These tiny vessels connect the arterioles and venules, allowing for the exchange of nutrients, waste products, and gases between the blood and the surrounding tissues.

The capillary wall is composed of a single layer of endothelial cells that are held together by tight junctions. The permeability of these walls varies depending on the size and charge of the molecules attempting to pass through. Small, uncharged molecules such as water, oxygen, and carbon dioxide can easily diffuse through the capillary wall, while larger or charged molecules such as proteins and large ions have more difficulty passing through.

Increased capillary permeability can occur in response to inflammation, infection, or injury, allowing larger molecules and immune cells to enter the surrounding tissues. This can lead to swelling (edema) and tissue damage if not controlled. Decreased capillary permeability, on the other hand, can lead to impaired nutrient exchange and tissue hypoxia.

Overall, the permeability of capillaries is a critical factor in maintaining the health and function of tissues throughout the body.

Respiratory Distress Syndrome, Adult (RDSa or ARDS), also known as Acute Respiratory Distress Syndrome, is a severe form of acute lung injury characterized by rapid onset of widespread inflammation in the lungs. This results in increased permeability of the alveolar-capillary membrane, pulmonary edema, and hypoxemia (low oxygen levels in the blood). The inflammation can be triggered by various direct or indirect insults to the lung, such as sepsis, pneumonia, trauma, or aspiration.

The hallmark of ARDS is the development of bilateral pulmonary infiltrates on chest X-ray, which can resemble pulmonary edema, but without evidence of increased left atrial pressure. The condition can progress rapidly and may require mechanical ventilation with positive end-expiratory pressure (PEEP) to maintain adequate oxygenation and prevent further lung injury.

The management of ARDS is primarily supportive, focusing on protecting the lungs from further injury, optimizing oxygenation, and providing adequate nutrition and treatment for any underlying conditions. The use of low tidal volumes and limiting plateau pressures during mechanical ventilation have been shown to improve outcomes in patients with ARDS.

BALB/c is an inbred strain of laboratory mouse that is widely used in biomedical research. The strain was developed at the Institute of Cancer Research in London by Henry Baldwin and his colleagues in the 1920s, and it has since become one of the most commonly used inbred strains in the world.

BALB/c mice are characterized by their black coat color, which is determined by a recessive allele at the tyrosinase locus. They are also known for their docile and friendly temperament, making them easy to handle and work with in the laboratory.

One of the key features of BALB/c mice that makes them useful for research is their susceptibility to certain types of tumors and immune responses. For example, they are highly susceptible to developing mammary tumors, which can be induced by chemical carcinogens or viral infection. They also have a strong Th2-biased immune response, which makes them useful models for studying allergic diseases and asthma.

BALB/c mice are also commonly used in studies of genetics, neuroscience, behavior, and infectious diseases. Because they are an inbred strain, they have a uniform genetic background, which makes it easier to control for genetic factors in experiments. Additionally, because they have been bred in the laboratory for many generations, they are highly standardized and reproducible, making them ideal subjects for scientific research.

Complement activation is the process by which the complement system, a part of the immune system, is activated to help eliminate pathogens and damaged cells from the body. The complement system consists of a group of proteins that work together to recognize and destroy foreign substances.

Activation of the complement system can occur through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteolytic reactions that ultimately result in the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis and removal.

The classical pathway is typically activated by the binding of antibodies to antigens on the surface of a pathogen or damaged cell. The lectin pathway is activated by the recognition of specific carbohydrate structures on the surface of microorganisms. The alternative pathway can be spontaneously activated and serves as an amplification loop for both the classical and lectin pathways.

Complement activation plays a crucial role in the immune response, but uncontrolled or excessive activation can also lead to tissue damage and inflammation. Dysregulation of complement activation has been implicated in various diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

The term "diving" is generally not used in the context of medical definitions. However, when referring to diving in relation to a medical or physiological context, it usually refers to the act of submerging the body underwater, typically for activities such as swimming, snorkeling, or scuba diving.

In a medical or physiological sense, diving can have specific effects on the human body due to changes in pressure, temperature, and exposure to water. Some of these effects include:

* Changes in lung volume and gas exchange due to increased ambient pressure at depth.
* Decompression sickness (DCS) or nitrogen narcosis, which can occur when dissolved gases form bubbles in the body during ascent from a dive.
* Hypothermia, which can occur if the water is cold and the diver is not adequately insulated.
* Barotrauma, which can occur due to pressure differences between the middle ear or sinuses and the surrounding environment.
* Other medical conditions such as seizures or heart problems can also be exacerbated by diving.

It's important for divers to undergo proper training and certification, follow safe diving practices, and monitor their health before and after dives to minimize the risks associated with diving.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

Endotoxemia is a medical condition characterized by the presence of endotoxins in the bloodstream. Endotoxins are toxic substances that are found in the cell walls of certain types of bacteria, particularly gram-negative bacteria. They are released into the circulation when the bacteria die or multiply, and can cause a variety of symptoms such as fever, inflammation, low blood pressure, and organ failure.

Endotoxemia is often seen in patients with severe bacterial infections, sepsis, or septic shock. It can also occur after certain medical procedures, such as surgery or dialysis, that may allow bacteria from the gut to enter the bloodstream. In some cases, endotoxemia may be a result of a condition called "leaky gut syndrome," in which the lining of the intestines becomes more permeable, allowing endotoxins and other harmful substances to pass into the bloodstream.

Endotoxemia can be diagnosed through various tests, including blood cultures, measurement of endotoxin levels in the blood, and assessment of inflammatory markers such as c-reactive protein (CRP) and procalcitonin (PCT). Treatment typically involves antibiotics to eliminate the underlying bacterial infection, as well as supportive care to manage symptoms and prevent complications.

Protein Kinase C (PKC) is a family of serine-threonine kinases that play crucial roles in various cellular signaling pathways. These enzymes are activated by second messengers such as diacylglycerol (DAG) and calcium ions (Ca2+), which result from the activation of cell surface receptors like G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs).

Once activated, PKC proteins phosphorylate downstream target proteins, thereby modulating their activities. This regulation is involved in numerous cellular processes, including cell growth, differentiation, apoptosis, and membrane trafficking. There are at least 10 isoforms of PKC, classified into three subfamilies based on their second messenger requirements and structural features: conventional (cPKC; α, βI, βII, and γ), novel (nPKC; δ, ε, η, and θ), and atypical (aPKC; ζ and ι/λ). Dysregulation of PKC signaling has been implicated in several diseases, such as cancer, diabetes, and neurological disorders.

Arachidonic acid is a type of polyunsaturated fatty acid that is found naturally in the body and in certain foods. It is an essential fatty acid, meaning that it cannot be produced by the human body and must be obtained through the diet. Arachidonic acid is a key component of cell membranes and plays a role in various physiological processes, including inflammation and blood clotting.

In the body, arachidonic acid is released from cell membranes in response to various stimuli, such as injury or infection. Once released, it can be converted into a variety of bioactive compounds, including prostaglandins, thromboxanes, and leukotrienes, which mediate various physiological responses, including inflammation, pain, fever, and blood clotting.

Arachidonic acid is found in high concentrations in animal products such as meat, poultry, fish, and eggs, as well as in some plant sources such as certain nuts and seeds. It is also available as a dietary supplement. However, it is important to note that excessive intake of arachidonic acid can contribute to the development of inflammation and other health problems, so it is recommended to consume this fatty acid in moderation as part of a balanced diet.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

An Enzyme-Linked Immunosorbent Assay (ELISA) is a type of analytical biochemistry assay used to detect and quantify the presence of a substance, typically a protein or peptide, in a liquid sample. It takes its name from the enzyme-linked antibodies used in the assay.

In an ELISA, the sample is added to a well containing a surface that has been treated to capture the target substance. If the target substance is present in the sample, it will bind to the surface. Next, an enzyme-linked antibody specific to the target substance is added. This antibody will bind to the captured target substance if it is present. After washing away any unbound material, a substrate for the enzyme is added. If the enzyme is present due to its linkage to the antibody, it will catalyze a reaction that produces a detectable signal, such as a color change or fluorescence. The intensity of this signal is proportional to the amount of target substance present in the sample, allowing for quantification.

ELISAs are widely used in research and clinical settings to detect and measure various substances, including hormones, viruses, and bacteria. They offer high sensitivity, specificity, and reproducibility, making them a reliable choice for many applications.

Cathepsin G is a serine protease, which is a type of enzyme that breaks down other proteins. It is produced and released by neutrophils, a type of white blood cell that plays an important role in the body's immune response to infection. Cathepsin G helps to digest and kill microorganisms that have invaded the body. It can also contribute to tissue damage and inflammation in certain diseases, such as rheumatoid arthritis and cystic fibrosis.

Recombinant proteins are artificially created proteins produced through the use of recombinant DNA technology. This process involves combining DNA molecules from different sources to create a new set of genes that encode for a specific protein. The resulting recombinant protein can then be expressed, purified, and used for various applications in research, medicine, and industry.

Recombinant proteins are widely used in biomedical research to study protein function, structure, and interactions. They are also used in the development of diagnostic tests, vaccines, and therapeutic drugs. For example, recombinant insulin is a common treatment for diabetes, while recombinant human growth hormone is used to treat growth disorders.

The production of recombinant proteins typically involves the use of host cells, such as bacteria, yeast, or mammalian cells, which are engineered to express the desired protein. The host cells are transformed with a plasmid vector containing the gene of interest, along with regulatory elements that control its expression. Once the host cells are cultured and the protein is expressed, it can be purified using various chromatography techniques.

Overall, recombinant proteins have revolutionized many areas of biology and medicine, enabling researchers to study and manipulate proteins in ways that were previously impossible.

Glucuronidase is an enzyme that catalyzes the hydrolysis of glucuronic acid from various substrates, including molecules that have been conjugated with glucuronic acid as part of the detoxification process in the body. This enzyme plays a role in the breakdown and elimination of certain drugs, toxins, and endogenous compounds, such as bilirubin. It is found in various tissues and organisms, including humans, bacteria, and insects. In clinical contexts, glucuronidase activity may be measured to assess liver function or to identify the presence of certain bacterial infections.

Inflammation mediators are substances that are released by the body in response to injury or infection, which contribute to the inflammatory response. These mediators include various chemical factors such as cytokines, chemokines, prostaglandins, leukotrienes, and histamine, among others. They play a crucial role in regulating the inflammatory process by attracting immune cells to the site of injury or infection, increasing blood flow to the area, and promoting the repair and healing of damaged tissues. However, an overactive or chronic inflammatory response can also contribute to the development of various diseases and conditions, such as autoimmune disorders, cardiovascular disease, and cancer.

Pneumonia is an infection or inflammation of the alveoli (tiny air sacs) in one or both lungs. It's often caused by bacteria, viruses, or fungi. Accumulated pus and fluid in these air sacs make it difficult to breathe, which can lead to coughing, chest pain, fever, and difficulty breathing. The severity of symptoms can vary from mild to life-threatening, depending on the underlying cause, the patient's overall health, and age. Pneumonia is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood tests. Treatment usually involves antibiotics for bacterial pneumonia, antivirals for viral pneumonia, and supportive care like oxygen therapy, hydration, and rest.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Toll-Like Receptor 4 (TLR4) is a type of protein found on the surface of some cells in the human body, including immune cells like macrophages and dendritic cells. It belongs to a class of proteins called pattern recognition receptors (PRRs), which play a crucial role in the innate immune system's response to infection.

TLR4 recognizes and responds to specific molecules found on gram-negative bacteria, such as lipopolysaccharide (LPS), also known as endotoxin. When TLR4 binds to LPS, it triggers a signaling cascade that leads to the activation of immune cells, production of pro-inflammatory cytokines and chemokines, and initiation of the adaptive immune response.

TLR4 is an essential component of the body's defense against gram-negative bacterial infections, but its overactivation can also contribute to the development of various inflammatory diseases, such as sepsis, atherosclerosis, and certain types of cancer.

Virulence factors in Bordetella pertussis, the bacterium that causes whooping cough, refer to the characteristics or components of the organism that contribute to its ability to cause disease. These virulence factors include:

1. Pertussis Toxin (PT): A protein exotoxin that inhibits the immune response and affects the nervous system, leading to the characteristic paroxysmal cough of whooping cough.
2. Adenylate Cyclase Toxin (ACT): A toxin that increases the levels of cAMP in host cells, disrupting their function and contributing to the pathogenesis of the disease.
3. Filamentous Hemagglutinin (FHA): A surface protein that allows the bacterium to adhere to host cells and evade the immune response.
4. Fimbriae: Hair-like appendages on the surface of the bacterium that facilitate adherence to host cells.
5. Pertactin (PRN): A surface protein that also contributes to adherence and is a common component of acellular pertussis vaccines.
6. Dermonecrotic Toxin: A toxin that causes localized tissue damage and necrosis, contributing to the inflammation and symptoms of whooping cough.
7. Tracheal Cytotoxin: A toxin that damages ciliated epithelial cells in the respiratory tract, impairing mucociliary clearance and increasing susceptibility to infection.

These virulence factors work together to enable Bordetella pertussis to colonize the respiratory tract, evade the host immune response, and cause the symptoms of whooping cough.

Antigens are substances (usually proteins) on the surface of cells, viruses, fungi, or bacteria that can be recognized by the immune system and provoke an immune response. In the context of differentiation, antigens refer to specific markers that identify the developmental stage or lineage of a cell.

Differentiation antigens are proteins or carbohydrates expressed on the surface of cells during various stages of differentiation, which can be used to distinguish between cells at different maturation stages or of different cell types. These antigens play an essential role in the immune system's ability to recognize and respond to abnormal or infected cells while sparing healthy cells.

Examples of differentiation antigens include:

1. CD (cluster of differentiation) molecules: A group of membrane proteins used to identify and define various cell types, such as T cells, B cells, natural killer cells, monocytes, and granulocytes.
2. Lineage-specific antigens: Antigens that are specific to certain cell lineages, such as CD3 for T cells or CD19 for B cells.
3. Maturation markers: Antigens that indicate the maturation stage of a cell, like CD34 and CD38 on hematopoietic stem cells.

Understanding differentiation antigens is crucial in immunology, cancer research, transplantation medicine, and vaccine development.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Cell surface receptors, also known as membrane receptors, are proteins located on the cell membrane that bind to specific molecules outside the cell, known as ligands. These receptors play a crucial role in signal transduction, which is the process of converting an extracellular signal into an intracellular response.

Cell surface receptors can be classified into several categories based on their structure and mechanism of action, including:

1. Ion channel receptors: These receptors contain a pore that opens to allow ions to flow across the cell membrane when they bind to their ligands. This ion flux can directly activate or inhibit various cellular processes.
2. G protein-coupled receptors (GPCRs): These receptors consist of seven transmembrane domains and are associated with heterotrimeric G proteins that modulate intracellular signaling pathways upon ligand binding.
3. Enzyme-linked receptors: These receptors possess an intrinsic enzymatic activity or are linked to an enzyme, which becomes activated when the receptor binds to its ligand. This activation can lead to the initiation of various signaling cascades within the cell.
4. Receptor tyrosine kinases (RTKs): These receptors contain intracellular tyrosine kinase domains that become activated upon ligand binding, leading to the phosphorylation and activation of downstream signaling molecules.
5. Integrins: These receptors are transmembrane proteins that mediate cell-cell or cell-matrix interactions by binding to extracellular matrix proteins or counter-receptors on adjacent cells. They play essential roles in cell adhesion, migration, and survival.

Cell surface receptors are involved in various physiological processes, including neurotransmission, hormone signaling, immune response, and cell growth and differentiation. Dysregulation of these receptors can contribute to the development of numerous diseases, such as cancer, diabetes, and neurological disorders.

Muramidase, also known as lysozyme, is an enzyme that hydrolyzes the glycosidic bond between N-acetylmuramic acid and N-acetylglucosamine in peptidoglycan, a polymer found in bacterial cell walls. This enzymatic activity plays a crucial role in the innate immune system by contributing to the destruction of invading bacteria. Muramidase is widely distributed in various tissues and bodily fluids, such as tears, saliva, and milk, and is also found in several types of white blood cells, including neutrophils and monocytes.

Pertussis toxin is an exotoxin produced by the bacterium Bordetella pertussis, which is responsible for causing whooping cough in humans. This toxin has several effects on the host organism, including:

1. Adenylyl cyclase activation: Pertussis toxin enters the host cell and modifies a specific G protein (Gαi), leading to the continuous activation of adenylyl cyclase. This results in increased levels of intracellular cAMP, which disrupts various cellular processes.
2. Inhibition of immune response: Pertussis toxin impairs the host's immune response by inhibiting the migration and function of immune cells like neutrophils and macrophages. It also interferes with antigen presentation and T-cell activation, making it difficult for the body to clear the infection.
3. Increased inflammation: The continuous activation of adenylyl cyclase by pertussis toxin leads to increased production of proinflammatory cytokines, contributing to the severe coughing fits and other symptoms associated with whooping cough.

Pertussis toxin is an essential virulence factor for Bordetella pertussis, and its effects contribute significantly to the pathogenesis of whooping cough. Vaccination against pertussis includes inactivated or genetically detoxified forms of pertussis toxin, which provide immunity without causing disease symptoms.

Chemokine (C-X-C motif) ligand 2, also known as CXCL2, is a small signaling protein that belongs to the chemokine family. Chemokines are a group of cytokines, or cell signaling molecules, that play crucial roles in immune responses and inflammation. They mediate their effects by interacting with specific receptors on the surface of target cells, guiding the migration of various immune cells to sites of infection, injury, or inflammation.

CXCL2 is primarily produced by activated monocytes, macrophages, and neutrophils, as well as endothelial cells, fibroblasts, and certain types of tumor cells. Its primary function is to attract and activate neutrophils, which are key effector cells in the early stages of inflammation and host defense against invading pathogens. CXCL2 exerts its effects by binding to its specific receptor, CXCR2, which is expressed on the surface of neutrophils and other immune cells.

In addition to its role in inflammation and immunity, CXCL2 has been implicated in various pathological conditions, including cancer, atherosclerosis, and autoimmune diseases. Its expression can be regulated by several factors, such as pro-inflammatory cytokines, bacterial products, and growth factors. Understanding the role of CXCL2 in health and disease may provide insights into the development of novel therapeutic strategies for treating inflammation-associated disorders.

Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.

A chronic granulomatous disease (CGD) is a group of rare inherited disorders that affect the body's ability to fight off certain types of bacterial and fungal infections. It is characterized by the formation of granulomas, which are abnormal masses or nodules composed of immune cells called macrophages that cluster together in an attempt to wall off and destroy the infectious agents.

In CGD, the macrophages have a genetic defect that prevents them from producing reactive oxygen species (ROS), which are molecules that help kill bacteria and fungi. As a result, the immune system is unable to effectively eliminate these pathogens, leading to chronic inflammation and the formation of granulomas.

CGD is typically diagnosed in childhood and can affect various organs and systems in the body, including the lungs, gastrointestinal tract, skin, and lymph nodes. Symptoms may include recurrent infections, fever, fatigue, weight loss, cough, diarrhea, and abdominal pain. Treatment typically involves antibiotics or antifungal medications to manage infections, as well as immunosuppressive therapy to control inflammation and prevent the formation of granulomas. In some cases, bone marrow transplantation may be considered as a curative treatment option.

Innate immunity, also known as non-specific immunity or natural immunity, is the inherent defense mechanism that provides immediate protection against potentially harmful pathogens (like bacteria, viruses, fungi, and parasites) without the need for prior exposure. This type of immunity is present from birth and does not adapt to specific threats over time.

Innate immune responses involve various mechanisms such as:

1. Physical barriers: Skin and mucous membranes prevent pathogens from entering the body.
2. Chemical barriers: Enzymes, stomach acid, and lysozyme in tears, saliva, and sweat help to destroy or inhibit the growth of microorganisms.
3. Cellular responses: Phagocytic cells (neutrophils, monocytes, macrophages) recognize and engulf foreign particles and pathogens, while natural killer (NK) cells target and eliminate virus-infected or cancerous cells.
4. Inflammatory response: When an infection occurs, the innate immune system triggers inflammation to increase blood flow, recruit immune cells, and remove damaged tissue.
5. Complement system: A group of proteins that work together to recognize and destroy pathogens directly or enhance phagocytosis by coating them with complement components (opsonization).

Innate immunity plays a crucial role in initiating the adaptive immune response, which is specific to particular pathogens and provides long-term protection through memory cells. Both innate and adaptive immunity work together to maintain overall immune homeostasis and protect the body from infections and diseases.

Cytosol refers to the liquid portion of the cytoplasm found within a eukaryotic cell, excluding the organelles and structures suspended in it. It is the site of various metabolic activities and contains a variety of ions, small molecules, and enzymes. The cytosol is where many biochemical reactions take place, including glycolysis, protein synthesis, and the regulation of cellular pH. It is also where some organelles, such as ribosomes and vesicles, are located. In contrast to the cytosol, the term "cytoplasm" refers to the entire contents of a cell, including both the cytosol and the organelles suspended within it.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) is a protein complex that plays a crucial role in regulating the immune response to infection and inflammation, as well as in cell survival, differentiation, and proliferation. It is composed of several subunits, including p50, p52, p65 (RelA), c-Rel, and RelB, which can form homodimers or heterodimers that bind to specific DNA sequences called κB sites in the promoter regions of target genes.

Under normal conditions, NF-κB is sequestered in the cytoplasm by inhibitory proteins known as IκBs (inhibitors of κB). However, upon stimulation by various signals such as cytokines, bacterial or viral products, and stress, IκBs are phosphorylated, ubiquitinated, and degraded, leading to the release and activation of NF-κB. Activated NF-κB then translocates to the nucleus, where it binds to κB sites and regulates the expression of target genes involved in inflammation, immunity, cell survival, and proliferation.

Dysregulation of NF-κB signaling has been implicated in various pathological conditions such as cancer, chronic inflammation, autoimmune diseases, and neurodegenerative disorders. Therefore, targeting NF-κB signaling has emerged as a potential therapeutic strategy for the treatment of these diseases.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Alkaloids are a type of naturally occurring organic compounds that contain mostly basic nitrogen atoms. They are often found in plants, and are known for their complex ring structures and diverse pharmacological activities. Many alkaloids have been used in medicine for their analgesic, anti-inflammatory, and therapeutic properties. Examples of alkaloids include morphine, quinine, nicotine, and caffeine.

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

Actin is a type of protein that forms part of the contractile apparatus in muscle cells, and is also found in various other cell types. It is a globular protein that polymerizes to form long filaments, which are important for many cellular processes such as cell division, cell motility, and the maintenance of cell shape. In muscle cells, actin filaments interact with another type of protein called myosin to enable muscle contraction. Actins can be further divided into different subtypes, including alpha-actin, beta-actin, and gamma-actin, which have distinct functions and expression patterns in the body.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Phosphatidylinositol 3-Kinases (PI3Ks) are a family of enzymes that play a crucial role in intracellular signal transduction. They phosphorylate the 3-hydroxyl group of the inositol ring in phosphatidylinositol and its derivatives, which results in the production of second messengers that regulate various cellular processes such as cell growth, proliferation, differentiation, motility, and survival.

PI3Ks are divided into three classes based on their structure and substrate specificity. Class I PI3Ks are further subdivided into two categories: class IA and class IB. Class IA PI3Ks are heterodimers consisting of a catalytic subunit (p110α, p110β, or p110δ) and a regulatory subunit (p85α, p85β, p55γ, or p50γ). They are primarily activated by receptor tyrosine kinases and G protein-coupled receptors. Class IB PI3Ks consist of a catalytic subunit (p110γ) and a regulatory subunit (p101 or p84/87). They are mainly activated by G protein-coupled receptors.

Dysregulation of PI3K signaling has been implicated in various human diseases, including cancer, diabetes, and autoimmune disorders. Therefore, PI3Ks have emerged as important targets for drug development in these areas.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

Alpha-defensins are a type of defensin, which are small cationic host defense peptides that contribute to the innate immune system's response to microbial invasion. They are primarily produced by neutrophils, but can also be expressed by some epithelial cells and other immune cells. Alpha-defensins have broad-spectrum antimicrobial activity against bacteria, fungi, and enveloped viruses. They also play a role in modulating the inflammatory response and wound healing. There are six human alpha-defensin genes (DEFA1 to DEFA6) that encode six different peptides: Human Neutrophil Peptides 1-4 (HNP1-4) and Human Defensin 5 and 6 (HD5 and HD6). The HNPs are stored in the azurophilic granules of neutrophils and are released upon their activation, while HD5 and HD6 are found in the Paneth cells of the small intestine.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

In 2004, Brinkmann and colleagues described a striking observation that activation of neutrophils causes the release of web- ... Neutrophils may be subdivided into segmented neutrophils and banded neutrophils (or bands). They form part of the ... Normally, neutrophils contain a nucleus divided into 2-5 lobes. Neutrophils are a type of phagocyte and are normally found in ... Gerasimov IG, Ignatov DI (2004). "[Neutrophil activation in vitro]". Tsitologiia. 46 (2): 155-158. PMID 15174354. Gerasimov IG ...
Prieto, JA; Panyutich, AV; Heine, RP (January 1997). "Neutrophil activation in preeclampsia. Are defensins and lactoferrin ... Human neutrophil peptides are also known as α-defensins. Human neutrophil-derived alpha-defensins (HNPs) are capable of ... Initially human alpha defensin peptides were isolated from the neutrophils and are thus called human neutrophil peptides. ... Human neutrophil peptides are found in human atherosclerotic arteries, inhibit LDL metabolism and fibrinolysis and promote Lp(a ...
Lee WL, Downey GP (February 2001). "Neutrophil activation and acute lung injury". Curr Opin Crit Care. 7 (1): 1-7. doi:10.1097/ ... Neutrophils do not return to the blood; they turn into pus cells and die. Mature neutrophils are smaller than monocytes and ... Neutrophils also play a key role in the development of most forms of acute lung injury. Here, activated neutrophils release the ... Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called ...
Knäuper V, Krämer S, Reinke H, Tschesche H (April 1990). "Characterization and activation of procollagenase from human ... Neutrophil+collagenase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (EC 3.4.24). ... Neutrophil collagenase (EC 3.4.24.34, matrix metalloproteinase 8, PMNL collagenase, MMP-8) is an enzyme. This enzyme catalyses ... Collagenase Hasty KA, Jeffrey JJ, Hibbs MS, Welgus HG (July 1987). "The collagen substrate specificity of human neutrophil ...
"The phosphorylation of the respiratory burst oxidase component p47phox during neutrophil activation. Phosphorylation of sites ... Neutrophil cytosolic factor 1 has been shown to interact with: Moesin, Neutrophil cytosolic factor 4, and RELA. GRCh38: Ensembl ... Neutrophil cytosol factor 1, also known as p47phox, is a protein that in humans is encoded by the NCF1 gene. The protein ... Gu Y, Xu YC, Wu RF, Nwariaku FE, Souza RF, Flores SC, Terada LS (May 2003). "p47phox participates in activation of RelA in ...
EID: 2-s2.0-0022340824 Pick, Edgar (2020). "Cell-Free NADPH Oxidase Activation Assays: A Triumph of Reductionism". Neutrophil. ... Pick, Edgar (1 January 2014). "Role of the Rho GTPase Rac in the activation of the phagocyte NADPH oxidase". Small GTPases. 5 ( ... Bromberg, Y., and Pick, E. Activation of NADPH-dependent superoxide production in a cell-free system by sodium dodecyl sulfate ... cite book}}: ,journal= ignored (help) Pick, E.; Kroizman, T.; Abo, A. (15 December 1989). "Activation of the superoxide-forming ...
Knäuper V, Murphy G, Tschesche H (January 1996). "Activation of human neutrophil procollagenase by stromelysin 2". European ... Nakamura H, Fujii Y, Ohuchi E, Yamamoto E, Okada Y (April 1998). "Activation of the precursor of human stromelysin 2 and its ... "Activation of type IV procollagenases by human tumor-associated trypsin-2". The Journal of Biological Chemistry. 272 (34): ...
Wientjes FB, Hsuan JJ, Totty NF, Segal AW (1993). "p40phox, a third cytosolic component of the activation complex of the NADPH ... Neutrophil cytosolic factor 4 has been shown to interact with Ku70, Neutrophil cytosolic factor 1 and Moesin. ENSG00000100365 ... It interacts primarily with neutrophil cytosolic factor 2 (NCF2/p67-phox) to form a complex with neutrophil cytosolic factor 1 ... Neutrophil cytosol factor 4 is a protein that in humans is encoded by the NCF4 gene. The protein encoded by this gene is a ...
Normal-density neutrophil activation correlated with MPO and PRTN3 mRNA. Increased autoantigen gene expression originating from ... The correlation between autoantigen gene expression and antibody-mediated normal-density neutrophil activation links gene ... highlights neutrophil heterogeneity where expression in normal-density neutrophils correlates with ANCA-induced activation". ... "Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro". Proceedings ...
Paulino EC, Steil AA, Jancar S (July 2006). "Effect of endothelins on human neutrophil activation by immune complexes". ... Some studies suggest that EDNRB activation by ET-2 regulates follicular rupture by antagonising effects of EDNRA stimulation. ...
... of activation. It shows a duplex role in affecting chemotaxis; while inactivating neutrophil CXCR2 receptor, generates an ... Staphopain A was shown to inhibit activation of the complement system activation by cleaving components that are part of all ... "Staphylococcus aureus Staphopain A inhibits CXCR2-dependent neutrophil activation and chemotaxis". The EMBO Journal. 31 (17): ... Staphopain A is elastinolytic to a degree fairly equal to that of neutrophil elastase, and has a very broad specificity ...
"Spatial and temporal analysis of Rac activation during live neutrophil chemotaxis". Curr. Biol. 12 (23): 2029-34. doi:10.1016/ ...
Dusi S, Rossi F (December 1993). "Activation of NADPH oxidase of human neutrophils involves the phosphorylation and the ... Neutrophil cytosol factor 2 is a protein that in humans is encoded by the NCF2 gene. This gene encodes neutrophil cytosolic ... "Entrez Gene: NCF2 neutrophil cytosolic factor 2 (65kDa, chronic granulomatous disease, autosomal 2)". Wientjes FB, Segal AW ( ... This oxidase produces a burst of superoxide which is delivered to the lumen of the neutrophil phagosome. Mutations in this gene ...
Schymeinsky J, Mócsai A, Walzog B (August 2007). "Neutrophil activation via beta2 integrins (CD11/CD18): molecular mechanisms ... However, other therapies using small allosteric CD11b agonists seem to be a promising tool as their activation of CD11b leads ... Consequently, this leads to a reduced activation of NF-κB and lower production of above-mentioned pro-inflammatory cytokines. ... Beside TLR signalling, CD11b also negatively regulates B cell receptor (BCR) signalling, and it suppresses T cell activation ...
October 2016). "Treatment with the GPR55 antagonist CID16020046 increases neutrophil activation in mouse atherogenesis". ... It was found to block a number of GPR55 mediated responses such as wound healing and activation of immune system T-cells and B- ...
... neutrophil activation and intravascular bubbles following open-water scuba diving. Goldman, S (2013); An improved new class of ... neutrophil activation and intravascular bubbles following open-water scuba diving". Undersea & Hyperbaric Medicine. 112 (8): ...
... neutrophil activation, and intravascular bubbles following open-water SCUBA diving". Journal of Applied Physiology. 112 (8): ...
Dwivedi, N., & Radic, M. (2012). Neutrophil activation and B-cell stimulation in the pathogenesis of Felty's syndrome. Polskie ... In Felty's syndrome, chronic activation of neutrophils progresses to neutropenia and unabated infections. Neutropenia is a ... Neutrophils are the most abundant cells among white blood cells and play an important role in the immune system by destroying ... Inflammatory chemicals draw neutrophils to the area where they congregate and fight infection. A decrease in the number of ...
"The phosphorylation of the respiratory burst oxidase component p47phox during neutrophil activation. Phosphorylation of sites ...
Schymeinsky J, Mócsai A, Walzog B (August 2007). "Neutrophil activation via beta2 integrins (CD11/CD18): molecular mechanisms ... Several transforming viruses contain "Immunoreceptor Tyrosine Activation Motifs" (ITAMs) which lead to activation of Syk ... However, activation of SYK relies less on phosphorylation by Src family kinases than ZAP70. SYK and ZAP70 share a common ... "Differential effect of the inhibition of Grb2-SH3 interactions in platelet activation induced by thrombin and by Fc receptor ...
Schymeinsky J, Mócsai A, Walzog B (August 2007). "Neutrophil activation via beta2 integrins (CD11/CD18): molecular mechanisms ... This is especially important for neutrophils, as cellular adhesion plays a large role in extravasation from the blood vessels. ... Gahmberg CG, Fagerholm S (August 2002). "Activation of leukocyte beta2-integrins". Vox Sanguinis. 83 Suppl 1: 355-8. doi: ... neutrophils and NK cells. LFA-1 is involved in adhesion and binding to antigen presenting cells through interactions with the ...
Neutrophils are also an important component of oncomodulin activation. Without neutrophils present, macrophages are less ... This is because neutrophils enter the area of inflammation before macrophages do. In addition to macrophages, neutrophils are ... "Neutrophils Express Oncomodulin and Promote Optic Nerve Regeneration". Journal of Neuroscience. 33 (37): 14816-14824. doi: ...
... resulting in the activation of macrophages. Macrophages secrete more IL-8, propagating the neutrophil-mediated inflammatory ... recruiting neutrophils. Neutrophil recruitment results in a very rapid onset of inflammation. Therefore, co-infection with ... Macrophages may be stimulated to secrete IL-8 by the same process as is seen in the gut, causing neutrophils to accumulate at ... Neutrophils produce pus in the dermal papillae, generating characteristic blisters. IL-31 accumulation at the blisters may ...
11 May 2022). "Acute inflammatory response via neutrophil activation protects against the development of chronic pain". Science ...
"Activation of human polymorphonuclear neutrophil functions by interferon-gamma and tumor necrosis factors". Journal of ... Formation of LT-α1-β2 complex enables binding to LT-β receptors and subsequent activation of signaling pathways. Activation of ... In order for activation to occur, LT-α must form a complex with LT-β to form the LT-α1-β2 complex. ... Activation of LT-β receptors is capable of inducing cell death of cancerous cells and suppressing tumor growth. The process of ...
2002). "Protein-tyrosine phosphatase MEG2 is expressed by human neutrophils. Localization to the phagosome and activation by ...
"Activation of human neutrophils by electronically transmitted phorbol-myristate acetate". Medical Hypotheses. 54 (1): 33-39. ... Thomas, Y.; Schiff, M.; Belkadi, L.; Jurgens, P.; Kahhak, L.; Benveniste, J. (2000). "Activation of Human Eurtrophils by ...
Thomas, Y.; Schiff, M.; Belkadi, L.; Jurgens, P.; Kahhak, L.; Benveniste, J. (2000). "Activation of human neutrophils by ...
13 (A163). J. Benveniste; Thomas Y; Schiff M; Belkadi L; Jurgens P; Kahhak L (2000). "Activation of human neutrophils by ... Thomas, Y.; Schiff, M.; Belkadi, L.; Jurgens, P.; Kahhak, L.; Benveniste, J. (2000). "Activation of Human Eurtrophils by ... "Histamine dilutions modulate basophil activation". Inflammation Research. Birkhäuser Basel. 53 (5): 181-188. doi:10.1007/s00011 ...
Activation of a nerve causes lower pH in the vesicles, and a larger pH in the cell. Calcium and hydrogen antiporters are ... Neutrophils, "degranulation," and "phagocytosis" from protein kinase C increases vATPase. vATPase activity creates immune ... V-ATPase dependent acidification is necessary for such intracellular processes as protein sorting, zymogen activation, receptor ... response against pathogens by macrophage activation. Dendritic cells require vATPase to mature. ENSG00000234920, ...
"Caspase-catalyzed cleavage and activation of Mst1 correlates with eosinophil but not neutrophil apoptosis". Blood. 99 (9): 3432 ... In addition to activation by straurosporine and FAS ligand, STK3 has been found to be activated through dissociation of GLRX ... Protein kinase activation is a frequent response of cells to treatment with growth factors, chemicals, heat shock, or apoptosis ... This protein kinase activation presumably allows cells to resist unfavorable environmental conditions. The yeast 'sterile 20' ( ...
Specific inhibition of leukotriene B4-induced neutrophil activation by LY223982.. W T Jackson, R J Boyd, L L Froelich, B E ... Specific inhibition of leukotriene B4-induced neutrophil activation by LY223982.. W T Jackson, R J Boyd, L L Froelich, B E ... Specific inhibition of leukotriene B4-induced neutrophil activation by LY223982.. W T Jackson, R J Boyd, L L Froelich, B E ... Specific inhibition of leukotriene B4-induced neutrophil activation by LY223982. Message Subject (Your Name) has forwarded a ...
Exaggerated neutrophil activation and formation of neutrophil extracellular traps (NETs) are reported in systemic sclerosis ( ... Factors promoting neutrophil activation in SSc remain largely unknown. Among the neutrophil activating factors, mitochondrial- ... Exaggerated neutrophil activation and formation of neutrophil extracellular traps (NETs) are reported in systemic sclerosis ( ... Factors promoting neutrophil activation in SSc remain largely unknown. Among the neutrophil activating factors, mitochondrial- ...
Lipopolysaccharide-mediated neutrophil vegf-a release in modulated by cannabinoid reception activation. ... Lipopolysaccharide-mediated neutrophil vegf-a release in modulated by cannabinoid reception activation. [Tesi di dottorato] ... Activation of cannabinoid receptor type-1 (CB1) and -2 (CB2) has been suggested as a new strategy to modulate in vitro and in ... The modulation of activation markers of PMNs by CB agonists was evaluated by flow cytometry. Angiogenesis in vitro was measured ...
Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid ... Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid ... Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid ...
... they may play roles as intercellular signal molecules in neutrophil activation. ... Neutrophil nucleotide receptors are coupled to guanine-nucleotide-binding proteins. As nucleotides are released from cells ... On the other hand, FMet-Leu-Phe primed neutrophils to generate O2- upon exposure to nucleotides. At a concentration of 100 ... potentiate activation of NADPH oxidase and degranulation by chemotactic peptides and induce aggregation of human neutrophils ...
... neutrophil activation and NET counts were increased in all 3 Plasmodium species. In falciparum malaria, neutrophil activation ... Neutrophil activation results in Plasmodium parasite killing in vitro, but neutrophil products including neutrophil ... Neutrophil activation and NETs were quantified by immunoassays and microscopy and correlated with parasite biomass and disease ... neutrophil activation and NET release may contribute to pathogenesis in severe falciparum malaria. Agents with potential to ...
... suggesting that HS costimulates neutrophils by means of P2 receptor activation. We conclude that hypertonic stress regulates ... indicating that HS suppresses neutrophils via A2 receptor activation. Antagonists of P2 receptors counteracted the enhancing ... Neutrophils express mRNA, encoding all known PI adenosine receptors (A1, A2a, A2b, and A3) and the nucleotide receptors P2Y2, ... Here, we report that HS dose-dependently releases adenosine 5-triphosphate (ATP) from neutrophils and that extracellular ATP ...
... : neutrophil reactivity intensity (NEUT-RI) and neutrophil granularity intensity (NEUT-GI) Why measure ... Neutrophil activation is an indicator of early innate immune response hence both, NEUT-GI and NEUT-RI, will be increased in ... Using Sysmexs XN-Series analysers, the activation status of neutrophils (NEUT-GI and NEUT-RI) and lymphocytes (RE-LYMP, AS- ... neutrophil activation?. The understanding neutrophil granulocytes role in inflammation has changed essentially over recent ...
Differential activation of neutrophil extracellular traps by specific periodontal bacteria. Free Radical Biology and Medicine. ... Differential activation of neutrophil extracellular traps by specific periodontal bacteria. Phillipa White, Paul Cooper, Mike ... Differential activation of neutrophil extracellular traps by specific periodontal bacteria. In: Free Radical Biology and ... White, P, Cooper, P, Milward, M, Milward, M & Chapple, I 2014, Differential activation of neutrophil extracellular traps by ...
Divergent mechanisms of inflammasome activation in neutrophil early response and inflammation S100A8 and S100A9 are cytosolic ... E-selectin-mediated rapid NLRP3 inflammasome activation regulates S100A8/S100A9 release from neutrophils via transient ... Neutrophils are a type of innate immune cell that contains distinctive cytoplasmic granules and a nucleus that is divided into ... Neutrophils can release S100A8/S100A9 as an alarmin via gasdermin D pores. Here, the authors untangle the regulatory mechanisms ...
Here we show that, in neutrophils, increases in Na+ (high salt, HS) impair the ability of human and murine neutrophils to ... Here we show that, in neutrophils, increases in Na+ (high salt, HS) impair the ability of human and murine neutrophils to ... Although neutrophils play an important role in fighting intruding invaders, the impact of increased Na+ on the antimicrobial ... Stimulation of neutrophils with phorbol-12-myristate-13-acetate (PMA) overcame high salt-induced impairment in ROS production ...
... determine the molecular mechanisms by which SOCE leads to neutrophil activation, 2) generate neutrophil lineage specific ... Uncontrolled activation of neutrophils is a major cause of tissue injury in inflammatory diseases such as arthritis, vasculitis ... Using stim1-/- bone marrow chimeric mice, we have found that loss of SOCE leads to a profound block in neutrophil activation. ... Our preliminary evidence suggests that PKC enzymes are the target of extracellular calcium during neutrophil activation. As a ...
Our data indicate that neutrophil activation is tightly regulated and requires activation by two simultaneous stimuli, which is ... consisting of a priming step followed by an activation step. Considering that neutrophil activation occurs ... read more in an ... Here, we indeed demonstrate that neutrophils require simultaneous ligation of two different receptors for efficient activation ... Neutrophils are abundantly present in the synovium and synovial fluid of patients suffering from arthritis. Neutrophils can be ...
However, despite studies that have referred to activation of neutrophils in DENV infections, the exact roles of neutrophils ... this confirmed in vivo neutrophil activation during DENV infection. Spontaneous decondensation of nuclei, an early event of ... Here, we explored the phenotypic and functional responses of neutrophils in a cohort of adult dengue patients. Results ... Our study suggests that neutrophils are involved in immunological responses to DENV infection. ...
... agnostic approach for the discovery and optimization of covalent inhibitors of human neutrophil elastase (hNE). Evaluation of ... Enzyme Activation / drug effects * Fluorides / chemistry* * Humans * Inhibitory Concentration 50 * Leukocyte Elastase / ... SuFEx-enabled, agnostic discovery of covalent inhibitors of human neutrophil elastase Proc Natl Acad Sci U S A. 2019 Sep 17;116 ... phenyl fluorosulfate with IC50 0.24 μM and greater than 833-fold selectivity over the homologous neutrophil serine protease, ...
Mincle activation enhances neutrophil migration and resistance to polymicrobial septic peritonitis. Wook Bin Lee, Ji Jing Yan, ... Lee, WB, Yan, JJ, Kang, JS, Zhang, Q, Choi, WY, Kim, LK & Kim, YJ 2017, Mincle activation enhances neutrophil migration and ... Mincle activation enhances neutrophil migration and resistance to polymicrobial septic peritonitis. / Lee, Wook Bin; Yan, Ji ... Mincle activation enhances neutrophil migration and resistance to polymicrobial septic peritonitis. In: Scientific reports. ...
In 2004, Brinkmann and colleagues described a striking observation that activation of neutrophils causes the release of web- ... Neutrophils may be subdivided into segmented neutrophils and banded neutrophils (or bands). They form part of the ... Normally, neutrophils contain a nucleus divided into 2-5 lobes. Neutrophils are a type of phagocyte and are normally found in ... Gerasimov IG, Ignatov DI (2004). "[Neutrophil activation in vitro]". Tsitologiia. 46 (2): 155-158. PMID 15174354. Gerasimov IG ...
Effects of skin-chamber fluids from human allergic reactions on neutrophil activation. In: The Journal of allergy and clinical ... Effects of skin-chamber fluids from human allergic reactions on neutrophil activation. The Journal of allergy and clinical ... Dive into the research topics of Effects of skin-chamber fluids from human allergic reactions on neutrophil activation. ... Effects of skin-chamber fluids from human allergic reactions on neutrophil activation. / Sato, Kaoru; Zweiman, Burton; ...
... suggesting a defect in β2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation ... suggesting a defect in β2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation ... suggesting a defect in β2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation ... suggesting a defect in β2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation ...
Activation of kinin B 1 receptors induces chemotaxis of human neutrophils. / Ehrenfeld, P.; Millan, C.; Matus, C. E. et al. En ... Activation of kinin B 1 receptors induces chemotaxis of human neutrophils. P. Ehrenfeld, C. Millan, C. E. Matus, J. E. Figueroa ... Activation of kinin B 1 receptors induces chemotaxis of human neutrophils. En: Journal of Leukocyte Biology. 2006 ; Vol. 80, N. ... Activation of kinin B 1 receptors induces chemotaxis of human neutrophils. Journal of Leukocyte Biology. 2006 jul.;80(1):117- ...
... following neutrophil activation, autocrine FXII binds to uPAR on the neutrophil surface in a zinc-dependent (Zn2+) manner. ... We found F12 mRNA in murine neutrophils and FXII protein in murine and human peripheral neutrophils. When neutrophils are ... First, neutrophil adhesion to fibrinogen was examined in WT and F12-/- cells. After fMLP stimulation, F12-/- neutrophil ... Activities of neutrophil-derived FXII are distinct from the function of plasma-derived FXII, which mediates contact activation ...
fMLP-induced neutrophil activation. Request a detailed protocol For in vitro fMLP stimulation, blood was stimulated with 100 nM ... of the in vitro neutrophil activation in blood with the bacterial wall-derived tripeptide fMLP confirmed that neutrophils were ... Such mechanical activation kinetics of neutrophils has not been reported before as the lower measurement rate of previous ... in line with the pronounced actin cortex that is a hallmark of neutrophil activation (Worthen et al., 1989; Rosenbluth et al., ...
... and activation-regulated chemokine; RANTES, regulated upon activation, normal t cell expressed and presumably secreted; MIP, ... macrophage inflammatory proteins; MIG, monokine-induced γ interferon; ENA, epithelial neutrophil-activating; GRO, growth ...
Abrogation of cathepsin C by Helicobacter pylori impairs neutrophil activation to promote gastric infection.. Liu, Yu Gang; ... Our findings identified a mechanism that H. pylori abrogate CtsC to impair neutrophil activation and to ensure persistence in ... Efforts to enable and boost this neutrophil activation pathway by active CtsC may therefore become valuable strategies in ... Abrogation of cathepsin C by Helicobacter pylori impairs neutrophil activation to promote gastric infection. ...
Ascaris suum-Derived Products Induce Human Neutrophil Activation via a G Protein-Coupled Receptor That Interacts with the ... Ascaris suum-Derived Products Induce Human Neutrophil Activation via a G Protein-Coupled Receptor That Interacts with the ... ABF also primed neutrophils for production of superoxide anions. Calcium mobilization in response to A. suum-derived products ... The effect of products from the nematodes Ascaris suum, Toxocara canis, and Anisakis simplex on human neutrophils were studied ...
Time profile of oxidative stress and neutrophil activation in ovine acute lung injury and sepsis. In: Shock. 2012 ; Vol. 37, No ... Time profile of oxidative stress and neutrophil activation in ovine acute lung injury and sepsis. Shock. 2012 May;37(5):468-472 ... Dive into the research topics of Time profile of oxidative stress and neutrophil activation in ovine acute lung injury and ... Time profile of oxidative stress and neutrophil activation in ovine acute lung injury and sepsis. / Lange, Matthias; Szabo, ...
Inhibition of Immune Complex Complement Activation And Neutrophil Extracellular Trap Formation By Peptide Inhibitor of ... in assays of immune complex-mediated complement activation in human sera and assays for NET formation by human neutrophils. The ... pathogenesis that have yet to be targeted therapeutically are immune complex-initiated complement activation and neutrophil ... Inhibition of Complement Activation, Myeloperoxidase, NET Formation And Oxidant.... A product of rational molecular design, PA- ...
... neutrophil and lymphocyte count, and neutrophil lymphocyte ratio (N/L ratio). ,i,Results,/i,. The mean N/L ratio, platelet ... i,Purpose,/i,. To demonstrate the relation between optic neuritis (ON) and systemic inflammation markers as neutrophil ... Platelet count and MPV are related to platelet activation [12]. MPV has an inverse correlation with acute, active inflammation ... WBC and neutrophil count were found significantly increased in MS patients (. , ). N/L ratio was in clinically definite MS ...
Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following scuba diving.Aug 14, 2015 ...
  • Neutrophils play a pivotal role within the periodontal lesion, where they have a cytotoxic arsenal at their disposal, including Reactive oxygen species (ROS) and release of neutrophil extracellular trap (NETs). (birmingham.ac.uk)
  • Spontaneous decondensation of nuclei, an early event of neutrophil extracellular trap (NET) formation, was also markedly increased in cells isolated from DENV-infected patients during the acute phase of the infection. (ox.ac.uk)
  • Abstract: Two major aspects of systemic lupus erythematosus (SLE) pathogenesis that have yet to be targeted therapeutically are immune complex-initiated complement activation and neutrophil extracellular trap (NET) formation by neutrophils. (realtalifesciences.com)
  • Neutrophils (also known as neutrocytes, heterophils or polymorphonuclear leukocytes) are a type of white blood cell. (wikipedia.org)
  • In addition to stimulating polymorphonuclear neutrophil (PMN) production, G-CSF may have significant effects on PMN function. (elsevierpure.com)
  • In addition, lung tissue was harvested at the respective time points for the measurement of malondialdehyde, interleukin 6, poly(ADP ribose), myeloperoxidase, and alveolar polymorphonuclear neutrophil score. (utmb.edu)
  • After static exposure to blood, strongly reduced platelet and increased polymorphonuclear neutrophil adhesion were observed on treated versus untreated surfaces. (nih.gov)
  • Comparisons of treated and untreated samples provide evidence for wettability being an important player for platelet adhesion, although multiple factors including surface oxide chemistry and charge might control polymorphonuclear neutrophil adhesion. (nih.gov)
  • Exaggerated neutrophil activation and formation of neutrophil extracellular traps (NETs) are reported in systemic sclerosis (SSc) but its involvement in SSc pathogenesis is not clear. (lu.se)
  • Neutrophils contribute to host defense through different mechanisms, including the formation of neutrophil extracellular traps (NETs). (frontiersin.org)
  • Neutrophils play important roles in host defense through different mechanisms, including the formation of neutrophil extracellular traps (NETs) ( 1 ). (frontiersin.org)
  • We monitored four parameters of activation: chemotaxis, cell polarization, intracellular Ca21 transients, and priming of superoxide anion production. (ed.ac.uk)
  • It has now been recognised that activated neutrophils secrete a variety of pro-inflammatory cytokines and surface molecules (MHCII) in a manner that allows presentation of antigen to, and activation of, T cells. (sysmex-mea.com)
  • In particular, the inflammatory response leads to injury of epithelial/endothelial cells and enhances the release of inflammatory mediators, including chemokines, cytokines and inflammatory cells (mainly neutrophils and macrophages , but also eosinophils , basophils, mast cells). (omicsonline.org)
  • Previously, we have shown in a mouse model that exposure to hog dust extract (HDE) collected from a CAFO results in the activation of protein kinase C (PKC), elevated lavage fluid cytokines/chemokines including interleukin-6 (IL-6), and the development of significant lung pathology. (cdc.gov)
  • Neutrophil nucleotide receptors are coupled to guanine-nucleotide-binding proteins. (uni-regensburg.de)
  • Antagonists of P2 receptors counteracted the enhancing effects of ATP, suggesting that HS costimulates neutrophils by means of P2 receptor activation. (escholarship.org)
  • We conclude that hypertonic stress regulates neutrophil function via a single molecule (ATP) and its metabolite (adenosine), using positive- and negative-feedback mechanisms through the activation of P2 and A2 receptors, respectively. (escholarship.org)
  • Here, we indeed demonstrate that neutrophils require simultaneous ligation of two different receptors for efficient activation. (uu.nl)
  • Different fragments, released from individual components during complement activation, operate by a non-cytolytic mechanism through specific receptors present on various cell types. (dadamo.com)
  • Adherence reaction mediated through the CR receptors on phagocytes lead to stimulation of phagocytosis, activation of metabolism and secretory function and movement of phagocytes into the inflammatory site. (dadamo.com)
  • The stimulatory substances, including opsonized particles, immune complexes, and chemotactic factors, bind to specific cell-surface receptors on the neutrophil. (bvsalud.org)
  • Whereas the chemotactic peptide, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMet-Leu-Phe), induced NADPH-oxidase-catalyzed superoxide (O2-) formation in human neutrophils, purine and pyrimidine nucleotides per se did not stimulate NADPH oxidase but enhanced O2- formation induced by submaximally and maximally stimulatory concentrations of fMet-Leu-Phe up to fivefold. (uni-regensburg.de)
  • Here, we report that HS dose-dependently releases adenosine 5'-triphosphate (ATP) from neutrophils and that extracellular ATP is rapidly converted to adenosine or activates p38 MAPK and enhances N-formyl-methionyl-lencyl-phenylalanine-induced superoxide formation. (escholarship.org)
  • Neutrophil total ROS and superoxide release were measured (2hours) by luminol and lucigenin-enhanced chemiluminescence respectively. (birmingham.ac.uk)
  • Collectively, these data demonstrate variability between periodontal bacteria in their ability to stimulate neutrophil total ROS production, superoxide and NET responses. (birmingham.ac.uk)
  • ABF also primed neutrophils for production of superoxide anions. (ed.ac.uk)
  • We have previously shown that hypertonic stress (HS) can suppress chemoattractant-induced neutrophil responses via cyclic adenosine monophosphate and enhance these responses through p38 mitogen-activated protein kinase (MAPK) activation. (escholarship.org)
  • Activation of cannabinoid receptor type-1 (CB1) and -2 (CB2) has been suggested as a new strategy to modulate in vitro and in vivo angiogenesis. (unina.it)
  • CB agonists modulated in vitro angiogenesis and endothelial permeability induced by supernatants of LPS-activated PMNs through the reduction of VEGF-A. Conclusions: Neutrophils play a central role in the control of bacterial infections and in the outcome of sepsis. (unina.it)
  • Neutrophil activation results in Plasmodium parasite killing in vitro, but neutrophil products including neutrophil extracellular traps (NETs) mediate host organ damage and may contribute to severe malaria. (tropmedres.ac)
  • To determine whether this activation is due to component(s) released early in these IgE-mediated reactions, we investigated the in vitro effects of skin chamber fluids (CF) on resting blood PMNs. (johnshopkins.edu)
  • In the presence of active CtsC, isolated human neutrophils activated via NF-κB pathway with augmented bactericidal capacity in vitro . (bvsalud.org)
  • Here, we report in vitro testing of peptide inhibitor of complement C1 (PIC1) in assays of immune complex-mediated complement activation in human sera and assays for NET formation by human neutrophils. (realtalifesciences.com)
  • We examined the direct effects of glucocorticoid treatment on neutrophil survival and function in vitro. (aai.org)
  • Uptake of this material caused lysosomal destabilization and inflammasome activation, corroborated by an increase in cathepsin B, caspase 1, and increased protein levels of IL-1â both in vitro and in vivo. (cdc.gov)
  • The observed results, which likely reflect a high exposure scenario, demonstrated acute inflammation, and toxicity in vitro and in vivo in part due to NLRP3 inflammasome activation. (cdc.gov)
  • Purified antibodies from some patients activated neutrophils in vitro and potentiated thrombosis when injected into mice. (cdc.gov)
  • The main cells of innate immunology are the phagocytes (neutrophils = PMN, monocytes = MØ, dendritic cells = DC). (scirp.org)
  • The understanding neutrophil granulocytes' role in inflammation has changed essentially over recent years. (sysmex-mea.com)
  • When adhered to a surface, neutrophil granulocytes have an average diameter of 12-15 micrometers (µm) in peripheral blood smears. (wikipedia.org)
  • the A2 receptor antagonists 8-(p-sulfophenyl)theophylline, 3,7-dimethyl-1-(2-propynyl)xanthine, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine, and 3-propylxanthine, but not A1 and A3 receptor antagonists, decreased the suppressive effect of HS, indicating that HS suppresses neutrophils via A2 receptor activation. (escholarship.org)
  • Transcriptome analyses revealed that trehalose dimycolate, a Mincle ligand, reduced the expression of G protein-coupled receptor kinase 2 (GRK2) in neutrophils. (elsevierpure.com)
  • Indeed, GRK2 expression was upregulated, but surface expression of the chemokine receptor CXCR2 was downregulated in blood neutrophils from Mincle-deficient mice with septic injury. (elsevierpure.com)
  • We analyzed the chemotactic effect of kinin B 1 receptor agonists on neutrophils isolated from peripheral blood of human healthy subjects. (uai.cl)
  • To test the effect of B 1 receptor agonists, each assay was carried out overnight at 37°C in 5% CO 2 -95% air on neutrophils primed with 1 ng/ml interleukin-1β. (uai.cl)
  • A generation of kinin B 1 receptor agonists during the early phase of acute inflammation may favor the recruitment of neutrophils to the inflammatory site. (uai.cl)
  • shows that tumour-associated neutrophils in glioblastoma originate from skull bone marrow and acquire an antigen-presenting cell phenotype intratumorally in the presence of local T cells. (nature.com)
  • Using stim1-/- bone marrow chimeric mice, we have found that loss of SOCE leads to a profound block in neutrophil activation. (ucsf.edu)
  • They are formed from stem cells in the bone marrow and differentiated into subpopulations of neutrophil-killers and neutrophil-cagers. (wikipedia.org)
  • A normal neutrophil should have 3-5 segments. (wikipedia.org)
  • TLR9 activation induces normal neutrophil responses in a child with IRAK-4 deficiency: involvement of the direct PI3K pathway. (lu.se)
  • The early view of the neutrophil playing only a passive role and simply responding to external signals has now been replaced by an appreciation that activated neutrophils can perform most of the functions of macrophages. (sysmex-mea.com)
  • Here the authors produce and characterize an intranasal liposomal vaccine against a peptide antigen from Streptococcus pyogenes and show that it induces a strong mucosal IgA response lasting for over one year, and that protection is dependent on cellular immunity mediated through IL-17, macrophages and neutrophils. (nature.com)
  • In macrophages, HS in combination with inflammatory stimuli leads to enhanced pro-inflammatory activation and increased antimicrobial capacity ( 8 , 12 , 13 , 24 , 25 ), while limiting their regulatory features ( 26 - 29 ). (frontiersin.org)
  • In the present study we assessed markers of neutrophil activation and NET formation in SSc patients in relation to markers of inflammation and disease phenotype. (lu.se)
  • The aim of the current study is to assess whether SSc patients have elevated levels of fMet and the role of fMet in neutrophil-mediated inflammation on SSc pathogenesis. (lu.se)
  • Our data for the first time implicates an important role for the mitochondrial component fMet in promoting neutrophil-mediated inflammation in SSc. (lu.se)
  • Background: Neutrophils (PMNs) are innate immune cells with primary roles in inflammation and in host defense against infections. (unina.it)
  • All parameters are part of the 'Extended Inflammation Parameters' package and are available after licence activation. (sysmex-mea.com)
  • The mechanistic functions of neutrophils in skin inflammation are not fully understood. (nature.com)
  • Here the authors use human psoriasis samples and a mouse model of skin inflammation to study neutrophils and find a CXCR4 hi population of NET-forming, phagocytic neutrophils whose induction depends on the transcription factor CREB1. (nature.com)
  • New findings suggest that neutrophil extracellular traps and their components have a functional role as triggers of IL-17-mediated inflammation and associated bone destruction in periodontitis. (nature.com)
  • Using gene knockout mice we have found that genetic deficiency of calcium signaling pathways in neutrophils results in a profound block in neutrophil activation and protection from tissue injury during inflammation. (ucsf.edu)
  • During the beginning (acute) phase of inflammation, particularly as a result of bacterial infection, environmental exposure, and some cancers, neutrophils are one of the first responders of inflammatory cells to migrate toward the site of inflammation. (wikipedia.org)
  • Neutrophils are chemoattracted to sites of inflammation by several stimuli. (uai.cl)
  • To demonstrate the relation between optic neuritis (ON) and systemic inflammation markers as neutrophil lymphocyte ratio (N/L ratio), platelet count, mean platelet volume (MPV), and red cell distribution width (RDW) and furthermore to evaluate the utilization of these markers to predict the frequency of the ON episodes. (hindawi.com)
  • Neutrophil lymphocyte ratio (N/L ratio) is an effective, easy, and inexpensive method to determine systemic inflammation in various diseases such as cancer, hypertension, diabetes mellitus, and coronary artery disorders [ 10 , 11 ]. (hindawi.com)
  • In a recent study [ 9 ] it was indicated for the first time that among various mediators involved in the inflammation-driven differentiation of fibroblast to an activated myofibroblast, a main architect is the neutrophil, a cell whose role in fibrosis was obscure up to now. (omicsonline.org)
  • Peripheral blood neutrophils were incubated with a panel of bacteria, including F. nucleatum and C. gingivalis. (birmingham.ac.uk)
  • We isolated human peripheral blood neutrophils and cultured them with various combinations of stimuli (GM-CSF, fMLF, TNF, and LPS). (uu.nl)
  • Objective: We sought to investigate whether activation of CB1 and CB2 by CB agonists modulate lipopolysaccharide (LPS)-mediated angiogenic activity of human PMNs. (unina.it)
  • The modulation of activation markers of PMNs by CB agonists was evaluated by flow cytometry. (unina.it)
  • We have found activated neutrophils (PMNs) in skin chambers overlying the site of ongoing human allergic reactions. (johnshopkins.edu)
  • Chemoattractant-induced adhesion of G-CSFR-deficient PMNs was significantly impaired, suggesting a defect in β2-integrin activation. (elsevierpure.com)
  • Additional activation of PMNs during intramedullary nailing (IMN) is thought to act as a second immunological hit. (biomedcentral.com)
  • Adenosine deaminase treatment abolished the suppressive effect of HS, indicating that HS inhibits neutrophils through adenosine generation. (escholarship.org)
  • Glucocorticoid treatment inhibits apoptosis in human neutrophils. (aai.org)
  • Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid arthritis. (bmj.com)
  • Neutrophils are abundantly present in the synovium and synovial fluid of patients suffering from arthritis. (uu.nl)
  • High salt caused reduced spontaneous movement, degranulation and impaired production of reactive oxygen species (ROS) while leaving neutrophil viability unchanged. (frontiersin.org)
  • Next, we evaluated essential neutrophil functions, including degranulation and ROS production using flow cytometry, mediator release using ELISA, NETosis by a live cell imaging method, phagocytosis by imaging flow cytometry, and extracellular vesicle (EV) release quantified by high-resolution flow cytometry. (uu.nl)
  • Exposure of neutrophils to any combination of stimuli, but not to single stimuli, resulted in significant degranulation, and mediator and EV release. (uu.nl)
  • The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. (bvsalud.org)
  • Store-operated calcium entry" (SOCE) into cells is one of the major intracellular signaling responses that induce neutrophil activation. (ucsf.edu)
  • S100A8 and S100A9 are cytosolic alarmins with autocrine functions that facilitate neutrophil recruitment. (nature.com)
  • Impaired neutrophil recruitment into the infection site is directly associated with severe sepsis, but the precise mechanism is unclear. (elsevierpure.com)
  • Mincle deficiency led to higher serum inflammatory cytokine levels and reduced bacterial clearance and neutrophil recruitment. (elsevierpure.com)
  • In both preventive and therapeutic treatments, ellagic acid reduced the vascular permeability changes and neutrophil recruitment to the bronchoalveolar lavage fluid (BALF) and to lung compared to the vehicle. (hindawi.com)
  • Specific inhibition of leukotriene B4-induced neutrophil activation by LY223982. (aspetjournals.org)
  • Whereas inhibition of p38/MAPK did not result in improved neutrophil defense, pharmacological blockade of the phagocyte oxidase (PHOX) or its genetic ablation mimicked the impaired antimicrobial activity detected under high salt conditions. (frontiersin.org)
  • Inhibition of Complement Activation, Myeloperoxidase, NET Formation And Oxidant. (realtalifesciences.com)
  • Four different glucocorticoids caused a dose-dependent inhibition of apoptosis leading to increased survival of neutrophils. (aai.org)
  • Recent evidence has suggested that certain compounds are effective in inhibiting neutrophil function and infiltration, and such inhibition is desirable for the treatment of patients with ALI and sepsis. (hindawi.com)
  • This process includes diffuse activation of inflammatory and coagulation cascades, vasodilation and vascular maldistribution, capillary endothelial leakage, and dysfunctional utilization of oxygen and nutrients at the cellular level. (medscape.com)
  • COVID-19, neutrophil extracellular traps and vascular complications in obstetric practice. (cdc.gov)
  • Here, the authors used mathematical tools combined with high resolution multiplex imaging mass cytometry to show an association between immature neutrophils, CD8 T cells and proliferating alveolar epithelial cells in areas of maximal alveolar damage in COVID-19 lungs. (nature.com)
  • Acute lung injury (ALI) is characterized by alveolar edema and uncontrolled neutrophil migration to the lung, and no specific therapy is still available. (hindawi.com)
  • ALI is characterised by alveolar edema and uncontrolled neutrophil migration to the lung. (hindawi.com)
  • Here, we explored the phenotypic and functional responses of neutrophils in a cohort of adult dengue patients. (ox.ac.uk)
  • Our study suggests that neutrophils are involved in immunological responses to DENV infection. (ox.ac.uk)
  • Moreover, CXCL2-mediated adhesion, chemotactic responses, and F-actin polymerization were reduced in Mincle-deficient neutrophils. (elsevierpure.com)
  • Aims/hypothesis NF-κB activation unites metabolic and inflammatory responses in many diseases yet less is known about the role that NF-κB plays in normal metabolism. (researchgate.net)
  • Markers of neutrophil activation (calprotectin, NETs) and levels of fMet were analyzed in plasma from two SSc cohorts (n=80 and n=20, respectively) using ELISA. (lu.se)
  • Neutrophil activation and NETs were quantified by immunoassays and microscopy and correlated with parasite biomass and disease severity. (tropmedres.ac)
  • Although NETs may inhibit parasite growth in asymptomatic P falciparum infection, neutrophil activation and NET release may contribute to pathogenesis in severe falciparum malaria. (tropmedres.ac)
  • The precise mechanism of how these genes may contribute to neutrophil function or the formation of NETs remains unclear and should be further investigated in experimental studies. (frontiersin.org)
  • NETs are released as a result of a unique form of cell death, where DNA coated with histones and anti-microbial proteins, such as neutrophil elastase and myeloperoxidase (MPO), form a web-like structure ( 1 ). (frontiersin.org)
  • Of the Stim and Orai proteins in mice, it is unclear which play the dominant role in SOCE in neutrophils. (ucsf.edu)
  • Our goal is to determine the mechanisms and proteins involved in SOCE in neutrophils, then ask whether targeting these proteins will reverse inflammatory disease. (ucsf.edu)
  • By studying these animals, we hope to define the target proteins inside neutrophils that are activated by calcium entry as well as develop new reagents to test whether therapeutic blockade of calcium entry can reverse ongoing inflammatory disease in mouse models. (ucsf.edu)
  • Fasting, on the other hand, strengthened the neutrophils' phagocytic capacity to engulf bacteria. (wikipedia.org)
  • Effects were attenuated in exposed NLRP3 knockout THP-1 cells, demonstrating inflammasome activation. (cdc.gov)
  • Neutrophil activation is an indicator of early innate immune response hence both, NEUT-GI and NEUT-RI, will be increased in such a condition. (sysmex-mea.com)
  • Neutrophils are a type of innate immune cell that contains distinctive cytoplasmic granules and a nucleus that is divided into three segments. (nature.com)
  • The focus of the research is to understand how activation of the host inflammatory response regulates bacterial colonization of the urinary tract. (oru.se)
  • As nucleotides are released from cells under physiological and pathological conditions, they may play roles as intercellular signal molecules in neutrophil activation. (uni-regensburg.de)
  • We will determine which of the Stim and Orai molecules are most important in neutrophils by development of neutrophil lineage specific mutants of stim1, stim2, orai1 and orai2 in mice. (ucsf.edu)
  • Finally, we found that fewer Mincle-deficient neutrophils infiltrated from the blood circulation into the peritoneal fluid in bacterial septic peritonitis compared with wild-type cells. (elsevierpure.com)
  • Introduction regulate choices of expressed genes as part of the macrophage/ neutrophil lineage. (lu.se)
  • this confirmed in vivo neutrophil activation during DENV infection. (ox.ac.uk)
  • These data indicate that glucocorticoids can augment the effector potential of neutrophils by prolonging their survival and functional responsiveness, and such treatment might be detrimental in vivo because of delay in neutrophil apoptosis and in ultimate clearance of them from tissues. (aai.org)
  • This was confirmed in vivo by acute increased bronchoalveolar lavage levels of lactate dehydrogenase, pulmonary neutrophil influx, loss in mitochondrial membrane potential and augmented levels of 4-hydroxynonenal. (cdc.gov)
  • Synthetic derivatization of the initial hit led to a more potent agent, 2-(fluorosulfonyl)phenyl fluorosulfate with IC 50 0.24 μM and greater than 833-fold selectivity over the homologous neutrophil serine protease, cathepsin G. The optimized, yet simple benzenoid probe only modified active hNE and not its denatured form. (nih.gov)
  • Abrogation of cathepsin C by Helicobacter pylori impairs neutrophil activation to promote gastric infection. (bvsalud.org)
  • Cathepsin C (CtsC) functions as a central coordinator for activation of many serine proteases in immune cells . (bvsalud.org)
  • 168 Up to 17% of female human neutrophil nuclei have a drumstick-shaped appendage which contains the inactivated X chromosome. (wikipedia.org)
  • Efforts to enable and boost this neutrophil activation pathway by active CtsC may therefore become valuable strategies in treating H. pylori infection . (bvsalud.org)
  • Antibody levels were associated with neutrophil and coagulation pathway activation. (cdc.gov)
  • It is also known that alcohol, at least in part, exerts its anti-inflammatory response via activation of the hypothalamic-pituitary-adrenal axis pathway resulting in increases of glucocorticoids [ 10 ]. (cdc.gov)
  • Neutrophils are rapidly recruited to infected tissues and can engulf bacteria directly or produce toxic antimicrobial mediators. (nature.com)
  • found that the capacity of neutrophils to engulf bacteria is reduced when simple sugars like glucose, fructose as well as sucrose, honey and orange juice were ingested, while the ingestion of starches had no effect. (wikipedia.org)
  • The subsequent neutrophil activation leads to tissue damage via the release of proteases, oxidants, and cationic peptides [ 3 ]. (hindawi.com)
  • Thus, our results indicate that Mincle plays an important role in neutrophil infiltration and suggest that Mincle signaling may provide a therapeutic target for treating sepsis. (elsevierpure.com)
  • Neutrophil Activation and Early Features of NET Formation Are Associated With Dengue Virus Infection in Human. (ox.ac.uk)
  • In patients with symptomatic malaria, neutrophil activation and NET counts were increased in all 3 Plasmodium species. (tropmedres.ac)
  • In falciparum malaria, neutrophil activation and NET counts positively correlated with parasite biomass (Spearman rho = 0.41, P = .005 and r2 = 0.26, P = .002, respectively) and were significantly increased in severe disease. (tropmedres.ac)
  • The stated normal range for human blood counts varies between laboratories, but a neutrophil count of 2.5-7.5 × 109/L is a standard normal range. (wikipedia.org)
  • Non-survivors (n=54, 42%) presented significant alterations in hematological and coagulation parameters at admission, such as increased in white blood cells (WBC), neutrophil, and band cell counts, as well as elevated prothrombin time (PT), activated partial thromboplastin time, and D-dimer levels. (bvsalud.org)
  • Based on the identified response functions, we clarified the profiles of how the morphology spatiotemporally changes in response to local and transient activation of Rac1 and Cdc42 and found that Rac1 and Cdc42 activation triggers laterally propagating membrane protrusion. (nature.com)
  • Rapid and transient activation of myelin basic protein kinase in tobacco leaves treated with hairpin from Erwinia amylovora . (springer.com)
  • By adjusting their oxide layer composition, substrates were generated which are suitable for endothelial cell growth and at the same time show an altered (reduced) blood contact activation. (nih.gov)
  • [ 1 ] Although initial research showed promise, the fetoplacental response to bypass was characterized by cytokine activation, endothelial dysfunction, and increased resistance in the placenta, with fetal hypoxia and demise as end results. (medscape.com)
  • In addition, progressive increases in markers of neutrophil accumulation in the lung were observed. (utmb.edu)
  • Stimulation of neutrophils with phorbol-12-myristate-13-acetate (PMA) overcame high salt-induced impairment in ROS production and restored antimicrobial activity of neutrophils. (frontiersin.org)
  • However, despite studies that have referred to activation of neutrophils in DENV infections, the exact roles of neutrophils remain elusive. (ox.ac.uk)
  • Additionally, plasma samples from SSc patients with high levels of fMet induced de novo neutrophil activation through FPR1-dependent mechanisms. (lu.se)
  • On the other hand, FMet-Leu-Phe primed neutrophils to generate O2- upon exposure to nucleotides. (uni-regensburg.de)
  • Among the neutrophil activating factors, mitochondrial-derived N-formyl methionine (fMet) has been reported in several autoinflammatory conditions. (lu.se)
  • Here we show that, in neutrophils, increases in Na + (high salt, HS) impair the ability of human and murine neutrophils to eliminate Escherichia coli and Staphylococcus aureus . (frontiersin.org)
  • Our findings identified a mechanism that H. pylori abrogate CtsC to impair neutrophil activation and to ensure persistence in gastric mucosa . (bvsalud.org)
  • Therefore, if the complexity of neutrophils increases upon a change in functionality, e.g. by toxic granulation or vacuolisation, the position of the neutrophil cloud in the scattergram is also affected. (sysmex-mea.com)
  • Our findings suggest that increases in local Na + represent an ionic checkpoint that prevents excessive ROS production of neutrophils, which decreases their antimicrobial potential and could potentially curtail ROS-mediated tissue damage. (frontiersin.org)
  • We report here a SuFEx-enabled, agnostic approach for the discovery and optimization of covalent inhibitors of human neutrophil elastase (hNE). (nih.gov)
  • In suspension, human neutrophils have an average diameter of 8.85 µm. (wikipedia.org)
  • The average lifespan of inactivated human neutrophils in the circulation has been reported by different approaches to be between 5 and 135 hours(5 days and 15 hours). (wikipedia.org)
  • PA-dPEG24 was also able to dose-dependently inhibit NET formation by human neutrophils stimulated by PMA, MPO, or immune complex activated human sera. (realtalifesciences.com)
  • The effect of products from the nematodes Ascaris suum, Toxocara canis, and Anisakis simplex on human neutrophils were studied. (ed.ac.uk)
  • Multitrauma patients were characterized by a marked activation of the systemic inflammatory response, associated with a systemic activation of the monocyte and PMN compartments. (biomedcentral.com)
  • We also found that neutrophils activated and cleared bacteria in active CtsC-injected mice and that there was no bactericidal capacity in mice that were simultaneously neutrophil -depleted by Ly6G antibody. (bvsalud.org)
  • The neutrophils (PMN) are our main blood cells to combat fungi, bacteria, and fibrin. (scirp.org)
  • The formation of oxidative stress in the lung and activation of neutrophils are major determinants in the development of respiratory failure after acute lung injury and sepsis. (utmb.edu)
  • The results from our model may enhance the understanding of the pathophysiological alterations after acute lung injury and sepsis and thus be useful in exploring therapeutic interventions directed at modifying the expression or activation of inflammatory mediators. (utmb.edu)
  • Collectively, these data demonstrate that selective defects in PMN activation are present in G-CSFR-deficient mice and indicate that G-CSF plays an important role in regulating PMN chemokine responsiveness. (elsevierpure.com)
  • Activation of the complement cascade, with the formation of the effector MAC unit, results in cytotoxic and cytolytic reactions. (dadamo.com)
  • Nonglucocorticoid steroids did not modulate apoptosis in neutrophils. (aai.org)