Neutrophils. Medical search

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.

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 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 movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.

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.

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.

The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).

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.

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.

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.

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.

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)

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.

Adherence of cells to surfaces or to other 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.

A serine protease found in the azurophil granules of NEUTROPHILS. It has an enzyme specificity similar to that of chymotrypsin C.

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 T-LYMPHOCYTES. These receptors also bind several other CXC CHEMOKINES.

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.

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.

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.

A CXC chemokine that is synthesized by activated MONOCYTES and NEUTROPHILS. It has specificity for CXCR2 RECEPTORS.

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.

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.

The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.

Condensed areas of cellular material that may be bounded by a membrane.

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)

Cell adhesion molecule and CD antigen that serves as a homing receptor for lymphocytes to lymph node high endothelial venules.

Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.

A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.

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.

Techniques used for determining the values of photometric parameters of light resulting from LUMINESCENCE.

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.

DEFENSINS found in azurophilic granules of neutrophils and in the secretory granules of intestinal PANETH CELLS.

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.

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.

A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines.

White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).

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.

The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.

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.

High-affinity G-protein-coupled receptors for INTERLEUKIN-8 present on NEUTROPHILS; MONOCYTES; and BASOPHILS.

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 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)

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.

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.

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 diverse family of extracellular proteins that bind to small hydrophobic molecules. They were originally characterized as transport proteins, however they may have additional roles such as taking part in the formation of macromolecular complexes with other proteins and binding to CELL SURFACE RECEPTORS.

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 decrease in the number of NEUTROPHILS found in the blood.

Disordered formation of various types of leukocytes or an abnormal accumulation or deficiency of these cells.

A cytotoxic member of the CYTOCHALASINS.

The movement of cells or organisms toward or away from a substance in response to its concentration gradient.

An oxyacid of chlorine (HClO) containing monovalent chlorine that acts as an oxidizing or reducing agent.

Group of chemokines with paired cysteines separated by a different amino acid. CXC chemokines are chemoattractants for neutrophils but not monocytes.

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.

Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.

Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin.

Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.

Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.

The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)

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.

Leukocytes with abundant granules in the cytoplasm. They are divided into three groups according to the staining properties of the granules: neutrophilic, eosinophilic, and basophilic. Mature granulocytes are the NEUTROPHILS; EOSINOPHILS; and BASOPHILS.

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.

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.

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 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.

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.

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.

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 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.

Elements of limited time intervals, contributing to particular results or situations.

Proteins that are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. These proteins can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumor markers.

The passage of cells across the layer of ENDOTHELIAL CELLS, i.e., the ENDOTHELIUM; or across the layer of EPITHELIAL CELLS, i.e. the EPITHELIUM.

Antibodies produced by a single clone of cells.

Movement of tethered, spherical LEUKOCYTES along the endothelial surface of the microvasculature. The tethering and rolling involves interaction with SELECTINS and other adhesion molecules in both the ENDOTHELIUM and leukocyte. The rolling leukocyte then becomes activated by CHEMOKINES, flattens out, and firmly adheres to the endothelial surface in preparation for transmigration through the interendothelial cell junction. (From Abbas, Cellular and Molecular Immunology, 3rd ed)

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.

Proteins prepared by recombinant DNA technology.

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.

Family of antimicrobial peptides that have been identified in humans, animals, and plants. They are thought to play a role in host defenses against infections, inflammation, wound repair, and acquired immunity.

The rate dynamics in chemical or physical systems.

A member of the MATRIX METALLOPROTEINASES that cleaves triple-helical COLLAGEN types I, II, and III.

A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissues. They function optimally within an acidic pH range. The cathepsins occur as a variety of enzyme subtypes including SERINE PROTEASES; ASPARTIC PROTEINASES; and CYSTEINE PROTEASES.

INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.

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.

Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.

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.

Effective in the initiation of protein synthesis. The initiating methionine residue enters the ribosome as N-formylmethionyl tRNA. This process occurs in Escherichia coli and other bacteria as well as in the mitochondria of eucaryotic cells.

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.

The relationship between the dose of an administered drug and the response of the organism to the drug.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

Family of proteins associated with the capacity of LEUKOCYTES to adhere to each other and to certain substrata, e.g., the C3bi component of complement. Members of this family are the LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; (LFA-1), the MACROPHAGE-1 ANTIGEN; (Mac-1), and the INTEGRIN ALPHAXBETA2 or p150,95 leukocyte adhesion protein. They all share a common beta-subunit which is the CD18 antigen. All three of the above antigens are absent in inherited LEUKOCYTE-ADHESION DEFICIENCY SYNDROME, which is characterized by recurrent bacterial infections, impaired pus formation, and wound healing as well as abnormalities in a wide spectrum of adherence-dependent functions of granulocytes, monocytes, and lymphoid cells.

The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.

The phenomenon by which dissociated cells intermixed in vitro tend to group themselves with cells of their own type.

Soluble mediators of the immune response that are neither antibodies nor complement. They are produced largely, but not exclusively, by monocytes and macrophages.

Assays that measure the rate of migration of LEUKOCYTES. They may involve a variety of techniques such as measuring the movement of leukocytes through substrates such as AGAROSE gels or the rate of exit of cells from a glass capillary.

Infection of the lung often accompanied by inflammation.

Colorless to yellow dye that is reducible to blue or black formazan crystals by certain cells; formerly used to distinguish between nonbacterial and bacterial diseases, the latter causing neutrophils to reduce the dye; used to confirm diagnosis of chronic granulomatous disease.

Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.

Cell adhesion molecule and CD antigen that mediates neutrophil, monocyte, and memory T-cell adhesion to cytokine-activated endothelial cells. E-selectin recognizes sialylated carbohydrate groups related to the Lewis X or Lewis A family.

A CXC chemokine that is predominantly expressed in EPITHELIAL CELLS. It has specificity for the CXCR2 RECEPTORS and is involved in the recruitment and activation of NEUTROPHILS.

A class of cell surface leukotriene receptors with a preference for leukotriene B4. Leukotriene B4 receptor activation influences chemotaxis, chemokinesis, adherence, enzyme release, oxidative bursts, and degranulation in polymorphonuclear leukocytes. There are at least two subtypes of these receptors. Some actions are mediated through the inositol phosphate and diacylglycerol second messenger systems.

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.

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.

Cytochromes (electron-transporting proteins) with protoheme (HEME B) as the prosthetic group.

The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).

Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.

Glycoproteins found on the membrane or surface of cells.

Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.

The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the STOMACH. The two sacs are connected by the foramen of Winslow, or epiploic foramen.

Cells that can carry out the process of PHAGOCYTOSIS.

A 13.2-kDa member of the S-100 family of calcium-binding proteins that can form homo- or heterocomplexes with CALGRANULIN A and a variety of other proteins. The calgranulin A/B heterodimer is known as LEUKOCYTE L1 ANTIGEN COMPLEX. Calgranulin B is expressed at high concentrations in GRANULOCYTES during early monocyte differentiation, and serum calgranulin B levels are elevated in many inflammatory disorders such as CYSTIC FIBROSIS.

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.

Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.

Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.

A decrease in the number of GRANULOCYTES; (BASOPHILS; EOSINOPHILS; and NEUTROPHILS).

A subclass of lipid-linked proteins that contain a GLYCOSYLPHOSPHATIDYLINOSITOL LINKAGE which holds them to the CELL MEMBRANE.

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.

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.

A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.

Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.

A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.

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).

Organic esters of thioglycolic acid (HS-CH2COOH).

Phenomenon of cell-mediated immunity measured by in vitro inhibition of the migration or phagocytosis of antigen-stimulated LEUKOCYTES or MACROPHAGES. Specific CELL MIGRATION ASSAYS have been developed to estimate levels of migration inhibitory factors, immune reactivity against tumor-associated antigens, and immunosuppressive effects of infectious microorganisms.

Cell surface proteins that bind LIPOXINS with high affinity and trigger intracellular changes influencing the behavior 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 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.

Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.

Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.

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.

Rare, autosomal recessive disorder caused by deficiency of the beta 2 integrin receptors (RECEPTORS, LEUKOCYTE-ADHESION) comprising the CD11/CD18 family of glycoproteins. The syndrome is characterized by abnormal adhesion-dependent functions, especially defective tissue emigration of neutrophils, leading to recurrent infection.

Molecules found on the surface of some, but not all, B-lymphocytes, T-lymphocytes, and macrophages, which recognize and combine with the Fc (crystallizable) portion of immunoglobulin molecules.

An enzyme that catalyzes the oxidation of arachidonic acid to yield 5-hydroperoxyarachidonate (5-HPETE) which is rapidly converted by a peroxidase to 5-hydroxy-6,8,11,14-eicosatetraenoate (5-HETE). The 5-hydroperoxides are preferentially formed in leukocytes.

The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.

An integrin heterodimer widely expressed on cells of hematopoietic origin. CD11A ANTIGEN comprises the alpha chain and the CD18 antigen (ANTIGENS, CD18) the beta chain. Lymphocyte function-associated antigen-1 is a major receptor of T-CELLS; B-CELLS; and GRANULOCYTES. It mediates the leukocyte adhesion reactions underlying cytolytic conjugate formation, helper T-cell interactions, and antibody-dependent killing by NATURAL KILLER CELLS and granulocytes. Intracellular adhesion molecule-1 has been defined as a ligand for lymphocyte function-associated antigen-1.

A technique to study CELL MIGRATION in the INFLAMMATION process or during immune reactions. After an area on the skin is abraded, the movement of cells in the area is followed via microscopic observation of the exudate through a coverslip or tissue culture chamber placed over the area.

Substances that reduce or suppress INFLAMMATION.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

The number of LEUKOCYTES and ERYTHROCYTES per unit volume in a sample of venous BLOOD. A complete blood count (CBC) also includes measurement of the HEMOGLOBIN; HEMATOCRIT; and ERYTHROCYTE INDICES.

A dermal inflammatory reaction produced under conditions of antibody excess, when a second injection of antigen produces intravascular antigen-antibody complexes which bind complement, causing cell clumping, endothelial damage, and vascular necrosis.

Round, granular, mononuclear phagocytes found in the alveoli of the lungs. They ingest small inhaled particles resulting in degradation and presentation of the antigen to immunocompetent cells.

Inflammation of the lung parenchyma that is caused by bacterial infections.

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.

Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.

Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.

Trihydroxy derivatives of eicosanoic acids. They are primarily derived from arachidonic acid, however eicosapentaenoic acid derivatives also exist. Many of them are naturally occurring mediators of immune regulation.

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.

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.

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.

Small cationic peptides that are an important component, in most species, of early innate and induced defenses against invading microbes. In animals they are found on mucosal surfaces, within phagocytic granules, and on the surface of the body. They are also found in insects and plants. Among others, this group includes the DEFENSINS, protegrins, tachyplesins, and thionins. They displace DIVALENT CATIONS from phosphate groups of MEMBRANE LIPIDS leading to disruption of the membrane.

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.

A sub-family of RHO GTP-BINDING PROTEINS that is involved in regulating the organization of cytoskeletal filaments. This enzyme was formerly listed as EC 3.6.1.47.

Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).

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.

Protein of the annexin family exhibiting lipid interaction and steroid-inducibility.

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.

The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.

A transient increase in the number of leukocytes in a body fluid.

A phosphatidylinositol 3-kinase subclass that includes enzymes formed through the association of a p110gamma catalytic subunit and one of the three regulatory subunits of 84, 87, and 101 kDa in size. This subclass of enzymes is a downstream target of G PROTEIN-COUPLED RECEPTORS.

The minute vessels that collect blood from the capillary plexuses and join together to form veins.

Material coughed up from the lungs and expectorated via the mouth. It contains MUCUS, cellular debris, and microorganisms. It may also contain blood or pus.

The cells found in the body fluid circulating throughout the CARDIOVASCULAR SYSTEM.

White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells.

Peptides composed of between two and twelve amino acids.

The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.

Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.

Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.

Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.

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.

Disease having a short and relatively severe course.

Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP.

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 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.

Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by NEUTROPHILS, or chronic and dominated by LYMPHOCYTES and MACROPHAGES.

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.

Washing out of the lungs with saline or mucolytic agents for diagnostic or therapeutic purposes. It is very useful in the diagnosis of diffuse pulmonary infiltrates in immunosuppressed patients.

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.

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.

A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.

The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.

A species of gram-negative, facultatively anaerobic, rod-shaped bacteria normally commensal in the flora of CATTLE and SHEEP. But under conditions of physical or PHYSIOLOGICAL STRESS, it can cause MASTITIS in sheep and SHIPPING FEVER or ENZOOTIC CALF PNEUMONIA in cattle. Its former name was Pasteurella haemolytica.

Established cell cultures that have the potential to propagate indefinitely.

An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.

Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.

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 chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).

A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).

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.

A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.

GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. (1/19639)

Granulocyte-macrophage colony-stimulating factor (GM-CSF) gene-targeted mice (GM-/-) cleared group B streptococcus (GBS) from the lungs more slowly than wild-type mice. Expression of GM-CSF in the respiratory epithelium of GM-/- mice improved bacterial clearance to levels greater than that in wild-type GM+/+ mice. Acute aerosolization of GM-CSF to GM+/+ mice significantly enhanced clearance of GBS at 24 hours. GBS infection was associated with increased neutrophilic infiltration in lungs of GM-/- mice, while macrophage infiltrates predominated in wild-type mice, suggesting an abnormality in macrophage clearance of bacteria in the absence of GM-CSF. While phagocytosis of GBS was unaltered, production of superoxide radicals and hydrogen peroxide was markedly deficient in macrophages from GM-/- mice. Lipid peroxidation, assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice. GM-CSF plays an important role in GBS clearance in vivo, mediated in part by its role in enhancing superoxide and hydrogen peroxide production and bacterial killing by alveolar macrophages. (+info)

Interaction of inflammatory cells and oral microorganisms. II. Modulation of rabbit polymorphonuclear leukocyte hydrolase release by polysaccharides in response to Streptococcus mutans and Streptococcus sanguis. (2/19639)

The release of lysosomal hydrolases from polymorphonuclear leukocytes (PMNs) has been postulated in the pathogenesis of tissue injury in periodontal disease. In the present study, lysosomal enzyme release was monitored from rabbit peritoneal exudate PMNs exposed to Streptocccus mutans or Streptococcus sanguis. S. mutans grown in brain heart infusion (BHI) broth failed to promote significant PMN enzyme release. S. sanguis grown in BHI broth, although more effective than S. mutants, was a weak stimulus for promotion of PMN hydrolase release. Preincubation of washed, viable S. mutans in sucrose or in different-molecular-weight dextrans resulted in the ability of the organisms to provoke PMN release reactions. This effect could bot be demonstrated with boiled or trypsinized S. mutans or with viable S. sanguis. However, when grown in BHI broth supplemented with sucrose, but not with glucose, both S. mutans and S. sanguis triggered discharge of PMN enzymes. The mechanism(s) whereby dextran or sucrose modulates PMN-bacterial interaction may in some manner be related to promotion of microbial adhesiveness or aggregation by dextran and by bacterial synthesis of glucans from sucrose. (+info)

Interaction of inflammatory cells and oral microorganisms. III. Modulation of rabbit polymorphonuclear leukocyte hydrolase release response to Actinomyces viscosus and Streptococcus mutans by immunoglobulins and complement. (3/19639)

In the absence of antiserum, rabbit polymorphonuclear leukocytes (PMNs) released lysosomal enzymes in response to Actinomyces viscosus (19246) but not to Streptococcus mutans (6715). Antibodies had a marked modulating influence on these reactions. PMN hydrolase release was significantly enhanced to both organisms when specific rabbit antiserum and isolated immunoglobulin G (IgG) were included in the incubations. Immune complex F(ab')2 fragments of IgG directed against S. mutans agglutinated bacteria. Immune complexes consisting of S. mutans and F(ab')2 fragments of IgG directed against this organism were not effective as bacteria-IgG complexes in stimulating PMN release. The intensity of the release response to bacteria-IgG complexes was also diminished when PMNs were preincubated with isolated Fc fragments derived from IgG. Fresh serum as a source of complement components had no demonstrable effect on PMN release either alone or in conjuction with antiserum in these experiments. These data may be relevant to the mechanisms and consequences of the interaction of PMNs and plaque bacteria in the pathogenesis of periodontal disease. (+info)

Lung weight parallels disease severity in experimental coccidioidomycosis. (4/19639)

Evidence provided by histopathological study of lesions is a valuable adjunct for evaluating chemotherapeutic efficacy in experimental animal models, In addition, this should be correlated with a measure of disease severity in the same animal. The latter could be obtained by homogenization of infected organs and quantitative enumeration of viable cells of the etiological agent, but this would preclude histopathological studies in the same animal. Progression of disease in pulmonary infection is associated with replacement of air space by fluid, cells, and cellular debris. Therefore, an increase in lung weight should reflect severity of disease. Results with the murine model of coccidioidomycosis demonstrate that increasing lung weight parallels the increasing census of fungus cells in the lungs of both treated and nontreated infected mice. This was supported with evidence obtained from microscopic studies of lesions indicating that specific chemotherapy limited spread of the infection and inhibited multiplication of the fungus in the lung. Therefore, lung weight can be used as a measure of disease severity in the murine model of coccidioidomycosis. (+info)

Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils. (5/19639)

We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils. The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10. (+info)

Characterization and partial purification of a novel neutrophil membrane-associated kinase capable of phosphorylating the respiratory burst component p47phox. (6/19639)

The phosphorylation of p47phox is widely viewed as an important step in the activation of the neutrophil respiratory burst oxidase system. The exact nature of the kinase(s) responsible remains to be elucidated. We show here that such a kinase was detected on neutrophil membranes activated by either PMA or formyl-methionyl-leucyl-phenylalanine. This enzyme is not intrinsic to the neutrophil membrane and could be eluted with 0.5 M NaCl. The kinase activity was partially purified and was found not to be due to the presence of previously suggested kinases, including protein kinase C isotypes, mitogen-activated protein kinase and protein kinase B. Gel filtration and renaturation in substrate gels suggest a molecular mass of between 45 and 51 kDa. The kinase activity was independent of calcium and lipids but was potently inhibited by staurosporine. Treatment with protein phosphatase 2Ac suggested that the kinase was activated by serine/threonine phosphorylation. Phosphopeptide maps indicated that the kinase phosphorylated p47phox on similar sites to those found in vivo. These results indicate that activation of neutrophils by PMA results in the activation of a membrane-associated kinase that may play a part in the regulation of neutrophil NADPH oxidase through its ability to phosphorylate p47phox. (+info)

Non-serum-dependent chemotactic factors produced by Candida albicans stimulate chemotaxis by binding to the formyl peptide receptor on neutrophils and to an unknown receptor on macrophages. (7/19639)

Serum-free culture filtrates of six Candida species and Saccharomyces cerevisiae were found to contain chemoattractants for human polymorphonuclear leukocytes (PMNs) and a mouse macrophage-like cell line, J774. The chemotactic factors differed for the PMN and J774 cells, however, in terms of heat stability, kinetics of liberation by the yeast cells, and divalent cation requirements for production. The chemoattractant in Candida albicans culture filtrates appeared to act through the formyl peptide receptor (FPR) of PMNs, since it was found to induce chemotaxis of Chinese hamster ovary (CHO) cells that were expressing the human FPR but did not induce chemotaxis of wild-type CHO cells. The C. albicans culture filtrates also induced migration of PMNs across confluent monolayers of a human gastrointestinal epithelial cell line, T84; migration occurred in the basolateral-to-apical direction but not the reverse direction, unless the epithelial tight junctions were disrupted. J774 cells did not migrate toward the formylated peptide (fMet-Leu-Phe; fMLF), and chemotaxis toward the C. albicans culture filtrate was not inhibited by an FPR antagonist (t-butoxycarbonyl-Met-Leu-Phe), suggesting that a different receptor mediated J774 cell chemotaxis. In conclusion, we have identified a receptor by which a non-serum-dependent chemotactic factor (NSCF) produced by C. albicans induced chemotaxis of PMNs. Additionally, we have shown that NSCF was active across epithelial monolayers. These findings suggest that NSCFs produced by C. albicans and other yeast species may influence host-pathogen interactions at the gastrointestinal tract mucosal surface by inducing phagocytic-cell infiltration. (+info)

Role of the extracellular signal-regulated protein kinase cascade in human neutrophil killing of Staphylococcus aureus and Candida albicans and in migration. (8/19639)

Killing of Staphylococcus aureus and Candida albicans by neutrophils involves adherence of the microorganisms, phagocytosis, and a collaborative action of oxygen reactive species and components of the granules. While a number of intracellular signalling pathways have been proposed to regulate neutrophil responses, the extent to which each pathway contributes to the killing of S. aureus and C. albicans has not been clearly defined. We have therefore examined the effect of blocking one such pathway, the extracellular signal-regulated protein kinase (ERK) cascade, using the specific inhibitor of the mitogen-activated protein kinase/ERK kinase, PD98059, on the ability of human neutrophils to kill S. aureus and C. albicans. Our data demonstrate the presence of ERK2 and a 43-kDa form of ERK but not ERK1 in human neutrophils. Upon stimulation with formyl methionyl leucyl phenylalanine (fMLP), the activities of both ERK2 and the 43-kDa form were stimulated. Despite abrogating the activity of both ERK forms, PD98059 only slightly reduced the ability of neutrophils to kill S. aureus or C. albicans. This is consistent with our finding that PD98059 had no effect on neutrophil adherence or degranulation, although pretreatment of neutrophils with PD98059 inhibited fMLP-stimulated superoxide production by 50%, suggesting that a change in superoxide production per se is not strictly correlated with microbicidal activity. However, fMLP-stimulated chemokinesis was markedly inhibited, while random migration and fMLP-stimulated chemotaxis were partially inhibited, by PD98059. These data demonstrate, for the first time, that the ERK cascade plays only a minor role in the microbicidal activity of neutrophils and that the ERK cascade is involved primarily in regulating neutrophil migration in response to fMLP. (+info)

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

Also known as: chronic granulomatous disease, CGD.

Symptoms of neutropenia may include recurring infections, fever, fatigue, weight loss, and swollen lymph nodes. The diagnosis is typically made through a blood test that measures the number of neutrophils in the blood.

Treatment options for neutropenia depend on the underlying cause but may include antibiotics, supportive care to manage symptoms, and in severe cases, bone marrow transplantation or granulocyte-colony stimulating factor (G-CSF) therapy to increase neutrophil production.

There are several types of leukocyte disorders, including:

1. Leukemia: a malignancy of the blood cells that can affect any type of blood cell, including white blood cells.
2. Neutropenia: a condition characterized by a low number of neutrophils (a type of white blood cell) in the blood.
3. Monocytopenia: a condition characterized by a low number of monocytes (a type of white blood cell) in the blood.
4. Lymphopenia: a condition characterized by a low number of lymphocytes (a type of white blood cell) in the blood.
5. Leukopenia: a condition characterized by a low number of all types of white blood cells in the blood.
6. Thalassemia: a genetic disorder that affects the production of hemoglobin, which is necessary for red blood cells to carry oxygen in the body.
7. Fanconi anemia: a rare genetic disorder that affects the production of white blood cells and increases the risk of cancer and other health problems.
8. Diamond-Blackfan anemia: a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
9. Chronic granulomatous disease (CGD): a condition caused by a defect in the production of a type of white blood cell called a granulocyte, which makes it difficult for the body to fight off infections.
10. Chediak-Higashi syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infections and other health problems.

Treatment for leukocyte disorders depends on the specific condition and may include medications, blood transfusions, or bone marrow transplantation. In some cases, the only effective treatment is a bone marrow transplant.

Inherited bone marrow failure syndromes (IBMFS) are a group of rare genetic disorders that affect the bone marrow's ability to produce blood cells, including red blood cells, white blood cells, and platelets. These disorders can lead to anemia, neutropenia, thrombocytopenia, and an increased risk of infections and cancer.

The following are some of the most common inherited bone marrow failure syndromes:

1. Fanconi anemia: a rare genetic disorder that affects the production of white blood cells and increases the risk of cancer and other health problems.
2. Diamond-Blackfan anemia: a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
3. Chronic granulomatous disease (CGD): a condition caused by a defect in the production of a type of white blood cell called a granulocyte, which makes it difficult for the body to fight off infections.
4. Chediak-Higashi syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infection and other health problems.
5. X-linked sideroblastic anemia (XLSA): a rare genetic disorder that affects the production of red blood cells and can also lead to neutropenia and other complications.
6. Leukocyte adhesion deficiency (LAD): a rare genetic disorder that affects the production of white blood cells and increases the risk of infection.
7. Wiskott-Aldrich syndrome: a rare genetic disorder that affects the production of white blood cells and increases the risk of infection and other health problems.
8. X-linked agammaglobulinemia (XLA): a rare genetic disorder that affects the production of antibodies and increases the risk of infections.
9. Common variable immunodeficiency (CVID): a condition caused by a defect in the production of antibodies, which makes it difficult for the body to fight off infections.
10. Ataxia-telangiectasia (AT): a rare genetic disorder that affects the production of immune cells and increases the risk of cancer and other health problems.

It is important to note that these are just a few examples of primary immunodeficiency diseases and there are many more types of disorders that can affect the immune system. Each type of primary immunodeficiency disease has its own set of symptoms and may require different treatments.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The symptoms of peritonitis can vary depending on the severity and location of the inflammation, but they may include:

* Abdominal pain and tenderness
* Fever
* Nausea and vomiting
* Diarrhea or constipation
* Loss of appetite
* Fatigue
* Weakness
* Low blood pressure

Peritonitis can be diagnosed through a physical examination, medical history, and diagnostic tests such as a CT scan, MRI or ultrasound. Treatment usually involves antibiotics to clear the infection and supportive care to manage symptoms. In severe cases, surgery may be required to remove any infected tissue or repair damaged organs.

Prompt medical attention is essential for effective treatment and prevention of complications such as sepsis, organ failure, and death.

Symptoms of pneumonia may include cough, fever, chills, difficulty breathing, and chest pain. In severe cases, pneumonia can lead to respiratory failure, sepsis, and even death.

There are several types of pneumonia, including:

1. Community-acquired pneumonia (CAP): This type of pneumonia is caused by bacteria or viruses and typically affects healthy people outside of hospitals.
2. Hospital-acquired pneumonia (HAP): This type of pneumonia is caused by bacteria or fungi and typically affects people who are hospitalized for other illnesses or injuries.
3. Aspiration pneumonia: This type of pneumonia is caused by food, liquids, or other foreign matter being inhaled into the lungs.
4. Pneumocystis pneumonia (PCP): This type of pneumonia is caused by a fungus and typically affects people with weakened immune systems, such as those with HIV/AIDS.
5. Viral pneumonia: This type of pneumonia is caused by viruses and can be more common in children and young adults.

Pneumonia is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood tests. Treatment may involve antibiotics, oxygen therapy, and supportive care to manage symptoms and help the patient recover. In severe cases, hospitalization may be necessary to provide more intensive care and monitoring.

Prevention of pneumonia includes vaccination against certain types of bacteria and viruses, good hygiene practices such as frequent handwashing, and avoiding close contact with people who are sick. Early detection and treatment can help reduce the risk of complications and improve outcomes for those affected by pneumonia.

This condition can be caused by various factors such as genetic mutations, infections, autoimmune disorders, and certain medications. In severe cases, agranulocytosis can lead to life-threatening infections that require prompt medical treatment.

Some of the common symptoms of agranulocytosis include fever, chills, sore throat, fatigue, and recurring infections. Diagnosis is typically made through blood tests that measure the number and function of white blood cells, including granulocytes. Treatment options for agranulocytosis depend on the underlying cause, but may include antibiotics, antiviral medications, and immunoglobulin replacement therapy in severe cases.

Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.

Reperfusion injury can be a complicating factor in various medical conditions, including:

1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.

Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.

Here are some key points to define sepsis:

1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.

Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.

The symptoms of ALI can vary depending on the severity of the condition, but may include:

* Shortness of breath (dyspnea)
* Chest pain or tightness (pleurisy)
* Cough, which may produce mucus or pus
* Fatigue, confusion, or disorientation
* Low oxygen levels in the blood (hypoxia)

If left untreated, ALI can progress to a more severe condition called acute respiratory distress syndrome (ARDS), which can be fatal. Treatment for ALI typically involves supportive care, such as mechanical ventilation, medications to manage inflammation and fluid buildup in the lungs, and management of underlying causes. In severe cases, extracorporeal membrane oxygenation (ECMO) or lung transplantation may be necessary.

It's important to note that ALI can occur in people of all ages and can be caused by a variety of factors, so it's important to seek medical attention right away if you or someone you know is experiencing symptoms of the condition.

These proteins are essential for white blood cells to stick together and migrate through the blood vessels into tissues, where they can fight off infections. The symptoms of Leukocyte Adhesion Deficiency syndrome vary depending on which gene is mutated and the severity of the mutation.

Some of the common symptoms include recurrent or persistent infections, poor wound healing, delayed development of the skin and mucous membranes, and difficulty fighting off certain types of bacteria, viruses, and fungi. The diagnosis of Leukocyte Adhesion Deficiency syndrome is based on a combination of clinical findings, laboratory tests that measure the function of white blood cells, and genetic analysis that identifies mutations in one of the genes involved in leukocyte adhesion.

Treatment for Leukocyte Adhesion Deficiency syndrome usually involves antibiotics to prevent or treat infections, topical creams or ointments to promote wound healing, and occasionally immunoglobulin replacement therapy to boost the immune system.

Several types of Leukocyte Adhesion Deficiency syndrome exist, each caused by a mutation in a different gene involved in leukocyte adhesion. The most common form of this disorder is called LAMA2 deficiency or Hereditary Angioedema with Giant Lymph Node.

Overall, early diagnosis and appropriate treatment can help manage symptoms and prevent complications associated with Leukocyte Adhesion Deficiency syndrome.

Leukocyte adhesion deficiency (LAD) is a group of rare genetic disorders characterized by impaired leukocyte trafficking and immune dysfunction. The disorders are caused by mutations in genes encoding proteins involved in leukocyte adhesion and migration, such as integrins and chemokine receptors.

There are several types of LAD, each with distinct clinical features and symptoms. The most common form of the disorder is LAMA2 deficiency, which affects approximately 1 in 50,000 individuals worldwide. Other forms of LAD include CD1a and CD1b deficiencies, which are less common but can have overlapping clinical features with LAMA2 deficiency.

The primary symptom of LAD is recurrent skin infections, particularly in childhood. Patients may also experience respiratory infections, gastrointestinal infections, and abscesses. In addition, some patients with LAD may develop chronic inflammation and fibrosis, which can lead to severe complications such as renal failure or blindness.

The diagnosis of LAD is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include flow cytometry, which can assess leukocyte function and adhesion properties, and molecular genetic testing, which can identify mutations in genes encoding integrins or other adhesion molecules.

Treatment of LAD typically involves antibiotics for recurrent skin and soft tissue infections, as well as management of any underlying chronic inflammation or fibrosis. In some cases, bone marrow transplantation may be considered as a curative therapy.

Overall, LAD is a rare and complex disorder that requires careful diagnosis and management by a multidisciplinary team of healthcare professionals. With appropriate treatment, many patients with LAD can lead active and productive lives, although some may experience ongoing complications or lifelong immune dysfunction.

The Arthus reaction is named after French physician Louis-Jean-Baptiste Arthus, who first described the phenomenon in 1890. It is commonly seen in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune disorders.

The reaction occurs when antibodies bind to antigens, such as proteins or cells, on the surface of tissues. The binding of antibodies to antigens can activate complement proteins, which are a group of proteins that work together to destroy pathogens. In the case of the Arthus reaction, the activation of complement proteins leads to the formation of a membrane attack complex (MAC), which is composed of various proteins and can cause damage to tissues.

The Arthus reaction can cause a range of symptoms, including joint pain, swelling, and warmth, as well as fever and fatigue. In severe cases, it can lead to permanent joint damage and disability. Treatment options for the Arthus reaction include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive medications.

In summary, the Arthus reaction is an allergic response that occurs when antibodies bind to antigens and form immune complexes, leading to inflammation and tissue damage. It is commonly seen in autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and can cause a range of symptoms including joint pain and swelling, fever, and fatigue. Treatment options include NSAIDs, corticosteroids, and immunosuppressive medications.

The most common bacteria that cause pneumonia are Streptococcus pneumoniae (also known as pneumococcus), Haemophilus influenzae, and Staphylococcus aureus. These bacteria can infect the lungs through various routes, including respiratory droplets, contaminated food or water, or direct contact with an infected person.

Symptoms of pneumonia may include cough, fever, chills, shortness of breath, and chest pain. In severe cases, pneumonia can lead to serious complications such as respiratory failure, sepsis, and death.

Diagnosis of pneumonia typically involves a physical examination, medical history, and diagnostic tests such as chest X-rays or blood cultures. Treatment typically involves antibiotics to eliminate the infection, as well as supportive care to manage symptoms and prevent complications. Vaccines are also available to protect against certain types of bacterial pneumonia, particularly in children and older adults.

Preventative measures for bacterial pneumonia include:

* Getting vaccinated against Streptococcus pneumoniae and Haemophilus influenzae type b (Hib)
* Practicing good hygiene, such as washing hands regularly and covering the mouth and nose when coughing or sneezing
* Avoiding close contact with people who are sick
* Staying hydrated and getting enough rest
* Quitting smoking, if applicable
* Managing underlying medical conditions, such as diabetes or heart disease

It is important to seek medical attention promptly if symptoms of pneumonia develop, particularly in high-risk populations. Early diagnosis and treatment can help prevent serious complications and improve outcomes for patients with bacterial pneumonia.

White blood cells are an important part of the immune system and play a crucial role in fighting off infections and diseases. However, when there is an excessive increase in their numbers, it can lead to various complications, including:

1. Increased risk of infection: With too many white blood cells in the bloodstream, there is a higher chance of developing infections.
2. Inflammation: Excessive production of white blood cells can cause inflammation in various parts of the body.
3. Blood clotting disorders: White blood cells can clump together and form clots, which can lead to blockages in blood vessels.
4. Tissue damage: The excessive growth of white blood cells can cause damage to tissues and organs.
5. Bone marrow failure: Prolonged leukocytosis can lead to bone marrow failure, which can result in a decrease in the production of other blood cells, such as red blood cells and platelets.

There are several types of leukocytosis, including:

1. Reactive leukocytosis: This is the most common type and is caused by an infection or inflammation.
2. Chronic leukocytosis: This type is characterized by a persistent increase in white blood cells over a long period of time.
3. Acute leukocytosis: This type is characterized by a sudden and severe increase in white blood cells, often accompanied by other symptoms such as fever and fatigue.
4. Leukemia: This is a type of cancer that affects the bone marrow and blood cells. It can cause an abnormal increase in white blood cells.

Diagnosis of leukocytosis typically involves a physical examination, medical history, and laboratory tests such as complete blood count (CBC) and bone marrow biopsy. Treatment depends on the underlying cause and may include antibiotics for infections, steroids to reduce inflammation, or chemotherapy for leukemia. In some cases, no treatment is necessary if the condition resolves on its own.

There are several types of edema, including:

1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.

Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.

There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:

1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.

The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.

Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.

In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:

1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.

It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

1. Acute respiratory distress syndrome (ARDS): This is a severe and life-threatening condition that occurs when the lungs become inflamed and fill with fluid, making it difficult to breathe.
2. Pneumonia: This is an infection of the lungs that can cause inflammation and damage to the air sacs and lung tissue.
3. Aspiration pneumonitis: This occurs when food, liquid, or other foreign substances are inhaled into the lungs, causing inflammation and damage.
4. Chemical pneumonitis: This is caused by exposure to harmful chemicals or toxins that can damage the lungs and cause inflammation.
5. Radiation pneumonitis: This occurs when the lungs are exposed to high levels of radiation, causing damage and inflammation.
6. Lung fibrosis: This is a chronic condition in which the lungs become scarred and stiff, making it difficult to breathe.
7. Pulmonary embolism: This occurs when a blood clot forms in the lungs, blocking the flow of blood and oxygen to the heart and other organs.

Symptoms of lung injury can include:

* Shortness of breath
* Chest pain or tightness
* Coughing up blood or pus
* Fever
* Confusion or disorientation

Treatment for lung injury depends on the underlying cause and severity of the condition, and may include oxygen therapy, medications to reduce inflammation, antibiotics for infections, and mechanical ventilation in severe cases. In some cases, lung injury can be a life-threatening condition and may require hospitalization and intensive care.

The hallmark of Wegener Granulomatosis is the formation of granulomas, which are clusters of immune cells that form in response to infection or inflammation. In this condition, however, the granulomas are not caused by an infectious agent but rather by the body's own immune system attacking its own tissues.

The symptoms of Wegener Granulomatosis can vary depending on the organs affected and can include:

* Fever
* Joint pain
* Fatigue
* Weight loss
* Shortness of breath
* Chest pain
* Coughing up blood
* Abdominal pain
* Blood in urine or stool
* Headache

The exact cause of Wegener Granulomatosis is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves the use of corticosteroids and other immunosuppressive medications to reduce inflammation and prevent further damage to the body. In some cases, plasmapheresis (plasma exchange) may also be used to remove harmful antibodies from the blood.

Wegener Granulomatosis is a relatively rare condition, affecting approximately 2-4 people per million each year. It can occur at any age but is most commonly diagnosed in adults between the ages of 40 and 60. With early diagnosis and proper treatment, many people with Wegener Granulomatosis can experience a good outcome and improved quality of life. However, if left untreated, the condition can be fatal.

Some common examples of bacterial infections include:

1. Urinary tract infections (UTIs)
2. Respiratory infections such as pneumonia and bronchitis
3. Skin infections such as cellulitis and abscesses
4. Bone and joint infections such as osteomyelitis
5. Infected wounds or burns
6. Sexually transmitted infections (STIs) such as chlamydia and gonorrhea
7. Food poisoning caused by bacteria such as salmonella and E. coli.

In severe cases, bacterial infections can lead to life-threatening complications such as sepsis or blood poisoning. It is important to seek medical attention if symptoms persist or worsen over time. Proper diagnosis and treatment can help prevent these complications and ensure a full recovery.

Phagocyte bactericidal dysfunction can be caused by a variety of factors, including genetic mutations, exposure to toxins, or infections with certain viruses or other pathogens that interfere with phagocyte function.

The consequences of phagocyte bactericidal dysfunction can include increased susceptibility to infections and the development of persistent or chronic infections, which can lead to a range of health problems and diseases.

Phagocyte bactericidal dysfunction is an important area of research in immunology and infectious disease, as understanding the mechanisms that control phagocyte function can help us develop new therapies and treatments for infections and other immune-related disorders.

Some common types of lung diseases include:

1. Asthma: A chronic condition characterized by inflammation and narrowing of the airways, leading to wheezing, coughing, and shortness of breath.
2. Chronic Obstructive Pulmonary Disease (COPD): A progressive condition that causes chronic inflammation and damage to the airways and lungs, making it difficult to breathe.
3. Pneumonia: An infection of the lungs that can be caused by bacteria, viruses, or fungi, leading to fever, chills, coughing, and difficulty breathing.
4. Bronchiectasis: A condition where the airways are damaged and widened, leading to chronic infections and inflammation.
5. Pulmonary Fibrosis: A condition where the lungs become scarred and stiff, making it difficult to breathe.
6. Lung Cancer: A malignant tumor that develops in the lungs, often caused by smoking or exposure to carcinogens.
7. Cystic Fibrosis: A genetic disorder that affects the respiratory and digestive systems, leading to chronic infections and inflammation in the lungs.
8. Tuberculosis (TB): An infectious disease caused by Mycobacterium Tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
9. Pulmonary Embolism: A blockage in one of the arteries in the lungs, often caused by a blood clot that has traveled from another part of the body.
10. Sarcoidosis: An inflammatory disease that affects various organs in the body, including the lungs, leading to the formation of granulomas and scarring.

These are just a few examples of conditions that can affect the lungs and respiratory system. It's important to note that many of these conditions can be treated with medication, therapy, or surgery, but early detection is key to successful treatment outcomes.

In adults, RDS is less common than in newborns but can still occur in certain situations. These include:

* Sepsis (a severe infection that can cause inflammation throughout the body)
* Pneumonia or other respiratory infections
* Injury to the lung tissue, such as from a car accident or smoke inhalation
* Burns that cover a large portion of the body
* Certain medications, such as those used to treat cancer or autoimmune disorders.

Symptoms of RDS in adults can include:

* Shortness of breath
* Rapid breathing
* Chest tightness or pain
* Low oxygen levels in the blood
* Blue-tinged skin (cyanosis)
* Confusion or disorientation

Diagnosis of RDS in adults is typically made based on a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood gas analysis. Treatment may involve oxygen therapy, mechanical ventilation (a machine that helps the patient breathe), and medications to help increase surfactant production or reduce inflammation in the lungs. In severe cases, a lung transplant may be necessary.

Prevention of RDS in adults includes avoiding exposure to risk factors such as smoking and other pollutants, maintaining good overall health, and seeking prompt medical attention if any respiratory symptoms develop.

The primary symptom of CHS is a weakened immune system, which makes patients more susceptible to infections such as pneumonia and meningitis. Other common symptoms include:

* Easy bruising and bleeding
* Poor wound healing
* Recurring skin rashes
* Enlarged lymph nodes
* Joint pain and stiffness
* Vision loss or blindness

There is no cure for CHS, but bone marrow transplantation has been shown to be effective in improving the immune system and reducing the risk of complications. Treatment also includes antibiotics to prevent and treat infections, as well as other supportive therapies to manage symptoms such as joint pain and vision loss.

The prognosis for CHS is generally poor, with many patients dying before the age of 20 due to complications related to infection or organ failure. However, with early diagnosis and appropriate treatment, some patients have been able to survive into adulthood.

CHS is an autosomal recessive disorder, meaning that it is caused by mutations in both copies of the CHS1 gene. This means that children must inherit one mutated copy of the gene from each parent in order to develop the condition.

There are several other conditions that can cause similar symptoms to CHS, including:

* X-linked severe combined immunodeficiency (XSCID)
* Leukocyte adhesion deficiency (LAD)
* Chronic granulomatous disease (CGD)

It is important for healthcare providers to be aware of these conditions and to consider them in the differential diagnosis when evaluating patients with symptoms similar to those of CHS.

Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.

Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.

Symptoms of cystic fibrosis can vary from person to person, but may include:

* Persistent coughing and wheezing
* Thick, sticky mucus that clogs airways and can lead to respiratory infections
* Difficulty gaining weight or growing at the expected rate
* Intestinal blockages or digestive problems
* Fatty stools
* Nausea and vomiting
* Diarrhea
* Rectal prolapse
* Increased risk of liver disease and respiratory failure

Cystic fibrosis is usually diagnosed in infancy, and treatment typically includes a combination of medications, respiratory therapy, and other supportive care. Management of the disease focuses on controlling symptoms, preventing complications, and improving quality of life. With proper treatment and care, many people with cystic fibrosis can lead long, fulfilling lives.

In summary, cystic fibrosis is a genetic disorder that affects the respiratory, digestive, and reproductive systems, causing thick and sticky mucus to build up in these organs, leading to serious health problems. It can be diagnosed in infancy and managed with a combination of medications, respiratory therapy, and other supportive care.

Pseudomonas infections are challenging to treat due to the bacteria's ability to develop resistance against antibiotics. The treatment typically involves a combination of antibiotics and other supportive therapies, such as oxygen therapy or mechanical ventilation, to manage symptoms and prevent complications. In some cases, surgical intervention may be necessary to remove infected tissue or repair damaged organs.

There are several types of dermatitis, including:

1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.

Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.

Symptoms of pulmonary edema may include:

* Shortness of breath (dyspnea)
* Coughing up frothy sputum
* Chest pain or tightness
* Fatigue
* Confusion or disorientation

Pulmonary edema can be diagnosed through physical examination, chest x-rays, electrocardiogram (ECG), and blood tests. Treatment options include oxygen therapy, diuretics, and medications to manage underlying conditions such as heart failure or sepsis. In severe cases, hospitalization may be necessary to provide mechanical ventilation.

Prevention measures for pulmonary edema include managing underlying medical conditions, avoiding exposure to pollutants and allergens, and seeking prompt medical attention if symptoms persist or worsen over time.

In summary, pulmonary edema is a serious condition that can impair lung function and lead to shortness of breath, chest pain, and other respiratory symptoms. Prompt diagnosis and treatment are essential to prevent complications and improve outcomes for patients with this condition.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

Also known as: Corneal inflammation, Eye inflammation, Keratoconjunctivitis, Ocular inflammation.

The symptoms of hemorrhagic shock may include:

* Pale, cool, or clammy skin
* Fast heart rate
* Shallow breathing
* Confusion or loss of consciousness
* Decreased urine output

Treatment of hemorrhagic shock typically involves replacing lost blood volume with IV fluids and/or blood transfusions. In severe cases, medications such as vasopressors may be used to raise blood pressure and improve circulation. Surgical intervention may also be necessary to control the bleeding source.

The goal of treatment is to restore blood flow and oxygenation to vital organs, such as the brain, heart, and kidneys, and to prevent further bleeding and hypovolemia. Early recognition and aggressive treatment of hemorrhagic shock are critical to preventing severe complications and mortality.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

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.[citation needed] Neutrophils are a type of phagocyte and are ... Though neutrophils can kill many microbes, the interaction of neutrophils with microbes and molecules produced by microbes ... They are formed from stem cells in the bone marrow and differentiated into subpopulations of neutrophil-killers and neutrophil- ...

https://en.wikipedia.org/wiki/Neutrophil

Neutrophil+collagenase at the US 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 ... Hasty KA, Pourmotabbed TF, Goldberg GI, Thompson JP, Spinella DG, Stevens RM, Mainardi CL (July 1990). "Human neutrophil ...

https://en.wikipedia.org/wiki/Neutrophil_collagenase

... is a type of coordinated neutrophil movement that acts in response to acute tissue inflammation or ... Additionally, neutrophil death during a swarm releases more signaling factors to recruit more neutrophils so the initial amount ... In comparison, the neutrophil swarms resulting from the laser induced injury only recruited around 50-330 neutrophils which ... In the second stage, the pioneer neutrophils attract a second wave of neutrophils that come from more distant regions of the ...

https://en.wikipedia.org/wiki/Neutrophil_swarming

Normal neutrophils are uniform in size, with an apparent diameter of about 13 μm in a film. When stained, neutrophils have a ... Neutrophil hypersegmentation can be defined as the presence of neutrophils whose nuclei have six or more lobes or the presence ... A 1996 study performed in the United States found that blacks have a greater neutrophil segmentation than whites. Neutrophil ... Up to 8% of circulating neutrophils are unsegmented ('band' forms). The presence of hypersegmented neutrophils is an important ...

https://en.wikipedia.org/wiki/Hypersegmented_neutrophil

The gene encoding neutrophil elastase, ELA2, consists of five exons. Neutrophil elastase is closely related to other cytotoxic ... Neutrophil elastase is secreted by neutrophils during inflammation, and destroys bacteria and host tissue. It also localizes to ... There appear to be two forms of neutrophil elastase, termed IIa and IIb. In humans, neutrophil elastase is encoded by the ELANE ... Neutrophil elastase (EC 3.4.21.37, leukocyte elastase, ELANE, ELA2, elastase 2, neutrophil, elaszym, serine elastase, subtype ...

https://en.wikipedia.org/wiki/Neutrophil_elastase

Neutrophil oxidative burst test (or chronic granulomatous disease (CGD) test) is a measure of neutrophil oxidation and is a ... From total blood, neutrophils can be purified and the NADPH oxidase activity can be measured with different methods in these ... Neutrophil respiratory burst in term and preterm neonates without signs of infection and in those with increased levels of C- ... In the neutrophil oxidative burst test heparinized whole blood is incubated at 37 °C with phorbol myristate acetate (PMA), a ...

https://en.wikipedia.org/wiki/Neutrophil_oxidative_index

... (ANC) is a measure of the number of neutrophil granulocytes (also known as polymorphonuclear cells, ... PMN's, polys, granulocytes, segmented neutrophils or segs) present in the blood. Neutrophils are a type of white blood cell ... This is known as the "I/T ratio". Al-Gwaiz LA, Babay HH (2007). "The diagnostic value of absolute neutrophil count, band count ... Absolute Neutrophil Count (ANC) (All articles with unsourced statements, Articles with unsourced statements from July 2020, ...

https://en.wikipedia.org/wiki/Absolute_neutrophil_count

... is a condition caused by mutations in the Rac2 gene. Immunodeficiency with hyper-IgM List ... "Orphanet: Neutrophil immunodeficiency syndrome". www.orpha.net. Retrieved 18 March 2019. Rapini, Ronald P.; Bolognia, Jean L.; ...

https://en.wikipedia.org/wiki/Neutrophil_immunodeficiency_syndrome

... (NETs) are networks of extracellular fibers, primarily composed of DNA from neutrophils, which ... Its rapid formation and release does not result in neutrophil death. It has been noted that neutrophils can continue to ... NETs allow neutrophils to kill extracellular pathogens while minimizing damage to the host cells. Upon in vitro activation with ... This effect is seen not only with neutrophils in the blood, but also in various tissues such as the gut, lung, liver, and blood ...

https://en.wikipedia.org/wiki/Neutrophil_extracellular_traps

... 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 ... "Entrez Gene: NCF4 neutrophil cytosolic factor 4, 40kDa". Muise AM, Xu W, Guo CH, Walters TD, Wolters VM, Fattouh R, Lam GY, Hu ...

https://en.wikipedia.org/wiki/Neutrophil_cytosolic_factor_4

... however a lack of defensins and lactoferrin drastically weakens the neutrophil innate ability to fight infection. Neutrophils ... Neutrophils and eosinophils will contain hyposegmented nuclei (a pseudo-Pelger-Huet anomaly). A majority of patients with SGD ... The defect in CEBPE appears to block the ability of neutrophils to mature past the promyelocyte stage in bone marrow. Since ... Neutrophil-specific granule deficiency ( previously known as lactoferrin deficiency) is a rare congenital immunodeficiency ...

https://en.wikipedia.org/wiki/Neutrophil-specific_granule_deficiency

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 ... Overview of all the structural information available in the PDB for UniProt: P19878 (Neutrophil cytosol factor 2) at the PDBe- ...

https://en.wikipedia.org/wiki/Neutrophil_cytosolic_factor_2

1990). "Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro". ... Furthermore, neutrophils release chemoattractive signalling molecules that recruit more neutrophils to the endothelium, acting ... ANCAs induce excess activation of neutrophils, resulting in the production of neutrophil extracellular traps (NETs), which ... on ethanol-fixed neutrophils is used to detect ANCA, although formalin-fixed neutrophils may be used to help differentiate ANCA ...

https://en.wikipedia.org/wiki/Anti-neutrophil_cytoplasmic_antibody

Wang J (Jan 2014). "The clinical significance of tumor-infiltrating neutrophils and neutrophil-to-CD8+lymphocyte ratio in ... In medicine neutrophil to lymphocyte ratio (NLR) is used as a marker of subclinical inflammation. It is calculated by dividing ... Neutrophil to Lymphocyte ratio was first demonstrated as useful parameter after a correlation of a relationship between the ... Wang X (Mar 2014). "Neutrophil to lymphocyte ratio in relation to risk of all-cause mortality and cardiovascular events among ...

https://en.wikipedia.org/wiki/Neutrophil_to_lymphocyte_ratio

... 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 ... "Entrez Gene: NCF1 neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)". "Study of complex genetic ... Volpp BD, Nauseef WM, Clark RA (1988). "Two cytosolic neutrophil oxidase components absent in autosomal chronic granulomatous ...

https://en.wikipedia.org/wiki/Neutrophil_cytosolic_factor_1

This process characterizes neutrophils as a type of phagocyte. Neutrophils contain neutrophil extracellular traps (NETs), ... Neutrophils are a type of phagocyte, abundant in blood, that phagocytize pathogens in acute inflammation. Neutrophils, along ... After stimulation of the neutrophil response, neutrophils lose their shape, allowing euchromatin and heterochromatin to ... Neutrophils are some of the first immune cells to travel to sites of infection that aid in fighting infection by ingesting ...

https://en.wikipedia.org/wiki/Nonspecific_immune_cell

... neutrophils, dendritic cells, mast cells, eosinophils, basophils, etc.) in variable proportions. Their abundance varies with ... "high neutrophils". Science. 358 (6367): eaal5081. doi:10.1126/science.aal5081. PMC 6343476. PMID 29191879. Gentles AJ, Newman ...

https://en.wikipedia.org/wiki/Tumor-infiltrating_lymphocytes

Also present are neutrophils and red blood cells in large numbers. The red blood cells are due to the proliferation of vaginal ... Neutrophils are increased. Red blood cells may be absent or present. Bacteria is commonly observed. A smear made during late ... No neutrophils are seen unless there is inflammation. There is usually no mucous in the background. In diestrus, superficial ... Late-proestrus - there is a decrease in neutrophils because they are unable to cross the thickening vaginal wall. Cytology ...

https://en.wikipedia.org/wiki/Vaginal_cytology

van Rees DJ, Szilagyi K, Kuijpers TW, Matlung HL, van den Berg TK (April 2016). "Immunoreceptors on neutrophils". Seminars in ... self-antigens or self-structures that play major role in inhibiting harmful immune system activity by regulating neutrophils ...

https://en.wikipedia.org/wiki/Siglec

Segal AW (2005). "How neutrophils kill microbes". Annual Review of Immunology. 23: 197-223. doi:10.1146/annurev.immunol. ... platelets and polymorphonuclear neutrophils of patients with sickle cell disease exhibit oxidative stress that can be ...

https://en.wikipedia.org/wiki/Oxidative_stress

Sengeløv H (1996). "Complement receptors in neutrophils". Critical Reviews in Immunology. 15 (2): 107-31. doi:10.1615/ ...

https://en.wikipedia.org/wiki/C5a_receptor

Neutrophils carry MMP-9., which has also been shown to degrade occludin. This leads to further disruption of the BBB and BSCB ... The increase in blood-brain barrier and blood-spinal cord barrier permeability allows for more neutrophils to infiltrate the ... Gurney KJ, Estrada EY, Rosenberg GA (Jul 2006). "Blood-brain barrier disruption by stromelysin-1 facilitates neutrophil ... "Neutrophils mediate blood-spinal cord barrier disruption in demyelinating neuroinflammatory diseases". Journal of Immunology. ...

https://en.wikipedia.org/wiki/MMP3

Neutrophil: Methods and Protocols. Methods in Molecular Biology. Vol. 2087. pp. 325-411. doi:10.1007/978-1-0716-0154-9_23. ISBN ... EID: 2-s2.0-0022340824 Pick, Edgar (2020). "Cell-Free NADPH Oxidase Activation Assays: A Triumph of Reductionism". Neutrophil. ...

https://en.wikipedia.org/wiki/Edgar_Pick

... is leukocytosis of neutrophils, that is, a high number of neutrophils in the blood. Because neutrophils are the main type of ... A "left shift" refers to the presence of increased proportions of younger, less well differentiated neutrophils and neutrophil- ... Neutrophils are also increased in any acute inflammation, so will be raised after a heart attack, other infarct or burns. Some ... Neutrophils are the primary white blood cells that respond to a bacterial infection, so the most common cause of neutrophilia ...

https://en.wikipedia.org/wiki/Neutrophilia

A decrease in levels of neutrophils on lab tests is due to either decreased production of neutrophils or increased removal from ... Neither dead cell debris nor attacking microorganisms can be dealt with effectively by the neutrophils. Unlike neutrophils, ... Neutrophils are active in phagocytosing bacteria and are present in large amount in the pus of wounds. These cells are not able ... Neutrophils are the most common cell type seen in the early stages of acute inflammation. The average lifespan of inactivated ...

https://en.wikipedia.org/wiki/White_blood_cell

Attracts macrophages, monocytes and neutrophils. Macrophage inflammatory proteins ENSG00000277632, ENSG00000274221 GRCh38: ... "Macrophages secrete a novel heparin-binding protein with inflammatory and neutrophil chemokinetic properties". The Journal of ...

https://en.wikipedia.org/wiki/CCL3

PRTN3 is a serine protease enzyme expressed mainly in neutrophil granulocytes. Its exact role in the function of the neutrophil ... It is also the target of anti-neutrophil cytoplasmic antibodies (ANCAs) of the c-ANCA (cytoplasmic subtype) class, a type of ... Ohlsson K, Linder C, Rosengren M (July 1990). "Monoclonal antibodies specific for neutrophil proteinase 4. Production and use ... Kettritz R (September 2016). "Neutral serine proteases of neutrophils". Immunological Reviews. 273 (1): 232-48. doi:10.1111/imr ...

https://en.wikipedia.org/wiki/Proteinase_3

Neutrophils may fill some ducts. It is characterized as a "fissured" or "dried mud" appearance from excess keratin production ...

https://en.wikipedia.org/wiki/Stomatitis_nicotina

There is an accumulation of mononuclear cells and neutrophils around the blood vessels (perivascular) of the CNS. Meningitis is ... Typically small mature lymphocytes are the majority of cells seen, with monocytes and neutrophils making up the rest. ... CSF analysis shows predominantly neutrophils. In Beagles this condition is also known as Beagle pain syndrome. Eosinophilic ...

https://en.wikipedia.org/wiki/Granulomatous_meningoencephalitis

... neutrophils, basophils, monocytes, and eosinophils; or 2) lymphoid precursor cells which differentiate into T lymphocytes, B ...

https://en.wikipedia.org/wiki/Clonal_hypereosinophilia

Neutrophils are produced in the bone marrow and released into the bloodstream to travel ... Neutrophils are a type of white blood cell that is responsible for much of the bodys protection against infection. ... Neutrophils are a type of white blood cell that is responsible for much of the bodys protection against infection. Neutrophils ... Large numbers of immature forms of neutrophils, called neutrophilic band cells, are produced by the bone marrow when the demand ...

https://medlineplus.gov/ency/imagepages/19864.htm

Comprehensive characterization of neutrophil genome topology. Yina Zhu, Ke Gong, Matthew Denholtz, Vivek Chandra, Mark P. Kamps ... Comprehensive characterization of neutrophil genome topology Message Subject (Your Name) has forwarded a page to you from ...

https://www.biorxiv.org/content/10.1101/100198v1.article-info

Scientists have discovered a new isoform which could be involved in the pathogenesis of pulmonary emphysema.

https://rtmagazine.com/disorders-diseases/chronic-pulmonary-disorders/copd/emphysema-novel-neutrophil-elastase-isoform-discovered/

Addressing whether glucose homeostasis relates to signs of neutrophil mobilization in COPD ... Figure 3 Neutrophil concentrations (A) in BAL (n= 5-10) and (B) in blood samples of HNS, LTS and LTS+COPD (n= 5-10). Neutrophil ... Neutrophil Concentrations in Long-Term Smokers with COPD. The BAL and blood neutrophil concentrations were higher in LTS+COPD ... Given that neutrophil elastase and other serine proteinases, as well as gelatinases, are released by neutrophils in response to ...

https://www.dovepress.com/glucose-homeostasis-in-relation-to-neutrophil-mobilization-in-smokers--peer-reviewed-fulltext-article-COPD

Neutrophils and neutrophil elastase, metalloproteases, and oxidants have all been shown to play a role in the pathogenesis of ... CSM induces the release of mediators by human neutrophils. Neutrophils were isolated from buffy coats and incubated for 9 h ... c Neutrophils were preincubated with S (10-7 M) or FP (10-9 M) or in combination for 90 min and then activated with CSM (0.06 ... Neutrophils were isolated from buffy coats and treated with CSM (a) or pretreated for 90 min with salmeterol (10-8 and 10-7 M) ...

https://link.springer.com/article/10.1007/s00109-008-0360-0

The Absolute Neutrophil Count (ANC) is a calculated parameter based on the total number of white blood cells, the percentage of ... The Absolute Neutrophil Count (ANC) is a calculated parameter based on the total number of white blood cells, the percentage of ... neutrophils, and the percentage of band cells in a patients blood sample at a given time. It has been used as a parameter to ... neutrophils, and the percentage of band cells in a patients blood sample at a given time. It has been used as a parameter to ...

http://reference.medscape.com/calculator/absolute-neutrophil-count

Platelets Amplify Neutrophil Polarization Induced by the Thromboxane Mimetic U46619 MJ Buchanan; MJ Buchanan ... MJ Buchanan, N Garlick, J Cooper, L Horn, CJ Hawkey, AT Cole; Platelets Amplify Neutrophil Polarization Induced by the ...

https://portlandpress.com/clinsci/article-abstract/87/s31/24P/106400/Platelets-Amplify-Neutrophil-Polarization-Induced?redirectedFrom=fulltext

Buy human neutrophil Elasetase (ELA-2) antigen for research, life science and IVD manufacturing uses - Inquire for details! ... The neutrophil form of elastase is 218 amino acids long, with two asparagine-linked carbohydrate chains. Current studies show ... Neutrophils, also known as neutrophilic polymorphonuclear leukocytes, are the major class of white blood cell in human ... Home / Antigens / Enzymes / Antigens / Enzymes / Standards / Controls / Proteins / Neutrophil Elastase (ela-2) ...

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Role of the Neutrophil NADPH Oxidase and S100A8/A9 in the Pathophysiology of Chronic Inflammation. Written By ...

https://www.intechopen.com/chapters/31365

Neutrophil genes such as neutrophil elastase (ELANE), proteinase 3 (PRTN3), cathepsin G (CTSG), azurocidin (AZU1) and MPO are ... Neutrophils are the most abundant leukocytes in humans. In homeostatic conditions, up to 2 × 1011 neutrophils enter the blood ... We found that both H1.2 and H1.4-deficient cells downregulated neutrophil genes, such as MPO and neutrophil proteases among ... Here we used the human neutrophil-like cell line, PLB-985, to study neutrophil maturation and function. We performed a genome- ...

https://elifesciences.org/articles/52563

Metabolic fate of glutamine in lymphocytes, macrophages and neutrophils. R. Curi1, P. Newsholme2, T.C. Pithon-Curi1, M. Pires- ... The role of high rates of glutaminolysis (and glycolysis) in lymphocytes, macrophages, and neutrophils ... Fate of glutamine utilization by lymphocytes, macrophages and neutrophils. It was generally believed that lymphocytes, ... Neutrophils constitute 60% of the circulating leukocytes. They act as first-line-of-defense cells in plasma and perform ...

https://indexmedicus.afro.who.int/iah/fulltext/BJMBR/v32_1/text2.htm

... a significant enrichment in transcripts involved in immune response pathways especially those contributing to neutrophil (IL8) ... a significant enrichment in transcripts involved in immune response pathways especially those contributing to neutrophil (IL8) ... Neutrophils and Snail Orchestrate the Establishment of a Pro-tumor Microenvironment in Lung Cancer. Cell Rep (2017) 21(11):3190 ... Polarization of tumor-associated neutrophil phenotype by TGF-beta: "N1" versus "N2" TAN. Cancer Cell (2009) 16(3):183-94. doi: ...

https://www.frontiersin.org/articles/10.3389/fimmu.2020.569671/full

Objective Neutrophil infiltration into the synovial joint is a hallmark of rheumatoid arthritis (RA), a disease characterised ... Neutrophil extracellular trap-associated carbamylation and histones trigger osteoclast formation in rheumatoid arthritis ... Neutrophil extracellular trap-associated carbamylation and histones trigger osteoclast formation in rheumatoid arthritis ... However, the mechanisms by which neutrophils participate in bone destruction remain unclear. Carbamylation is a ...

https://ard.bmj.com/content/82/5/630.full

Thus, in neutrophils, beta (2) integrin-induced activation of p190RhoGAP requires a signal from a Src family tyrosine kinase, ... Thus, in neutrophils, beta (2) integrin-induced activation of p190RhoGAP requires a signal from a Src family tyrosine kinase, ... We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ... We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ...

https://lup.lub.lu.se/search/publication/18081955-679d-4f8b-aa8b-27b69763024d

More neutrophils are attracted, as seen by an increase in the neutrophil concentration in the damaged area. The neutrophils ... Neutrophils were present in a high concentration among the 3 cell types (neutrophils, lymphocytes and phagocytes) in only 7% of ... Neutrophils were the predominant cells in the smear (,35% of the total cell count including neutrophils, macrophages and ... Table 1 shows the neutrophil counts as a percentage of the total neutrophils, phagocytes and lymphocytes in the microscope ...

https://www.emro.who.int/emhj-volume-16-2010/volume-16-issue-10/article-07.html

Neutrophil Elastase/Elastase-2) ELISA Kit from Gentaur Elisa Kits. Cat Number: G-EC-05121. USA, UK & Europe Distribution. ... Rat NE/ELA2 (Neutrophil Elastase/Elastase-2) ELISA Kit , G-EC-05121. Gentaur Elisa ... Rat NE/ELA2 (Neutrophil Elastase/Elastase-2) ELISA Kit DataSheet. Citation #1. Citation #2 ... Rat NE/ELA2 (Neutrophil Elastase/Elastase-2) ELISA Kit , G-EC-05121 ...

https://caslab.com/rat-ne-ela2-neutrophil-elastase-elastase-2-elisa-kit-g-ec-05121/?setCurrencyId=3

Learn more by reading about this critical role for neutrophils in resistance to experimental infection with Burkholderia ... A critical role for neutrophils in resistance to experimental infection with Burkholderia pseudomallei. J Infect Dis 195: 99- ... A Critical Role for Neutrophils in Resistance to Experimental Infection with Burkholderia pseudomallei ... A critical role for neutrophils in resistance to experimental infection with Burkholderia pseudomallei. ...

https://www.soligenix.com/blog/resource/a-critical-role-for-neutrophils-in-resistance-to-experimental-infection-with-burkholderia-pseudomallei/

Although neutrophils are essential for protection against extracellular bacteria, neutrophil-dominated inflammation can ... As neutrophils have been reported to be the key effector cells for the clearance of PA, there was therefore the need to include ... However, neutrophils do not act in isolation, they respond to cues provided by other cells such as macrophages, which influence ... This work describes the development of a human macrophage/neutrophil infection assay and its use to model Th-1 (IFN-γ) - and Th ...

https://eprints.nottingham.ac.uk/46598/

Neutrophils Pancreatin - immunology Sex Factors Sweden Abstract. Islet autoantibodies (IAs) precede the clinical onset of type ... We conclude that the reduction in neutrophils and red blood cells in children with multiple IAs and HLA-DR3-DQ2/DR4-DQ8 ... The white blood cell and neutrophil counts were reduced in children with IAs, primarily in boys. In contrast, girls had lower ... Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish ...

https://arctichealth.org/en/permalink/ahliterature296968

neutrophil; inflammation; COPD; neutrophil apoptosis; efferocytosis; mouse lung injury model; zebrafish. Dates:. *Accepted: 4 ... Therapeutic induction of neutrophil apoptosis, an immunologically silent form of cell death, may be beneficial in these ... Neratinib upregulates efferocytosis and reduces the number of persisting neutrophil corpses in mouse models of acute, but not ... Previous research in our group identified ErbB inhibitors as able to induce neutrophil apoptosis and reduce neutrophilic ...

https://eprints.whiterose.ac.uk/189737/

The use of Neutrophils from FERMT3 patients elucidated the requirement of kindlen3-CD18 interaction for synapse formation and ... Neutrophil Trogocytosis blocked by Ancell anti-CD18 mAb and F(ab)2 reagents in a CD47-SIRPa checkpoint disrupted model. By ... The use of Neutrophils from FERMT3 patients elucidated the requirement of kindlen3-CD18 interaction for synapse formation and ... "Kindlin3-Dependent CD11b/CD18-Integrin Activation IsRequired for Potentiation of Neutrophil Cytotoxicity byCD47-SIRPa ...

https://ancell.com/neutrophil-trogocytosis-blocked-by-ancell-anti-cd18-mab-and-fab2-reagents-in-a-cd47-sirpa-checkpoint-disrupted-model/

... by neutrophils. Neutrophils can establish T-cell inhibition by (1) degranulation of granular constituents. The serine proteases ... Neutrophils possess the capacity to cross-prime CD8+ T-cells directly in a MHCI-dependent manner. (6) Release of microbial ... Dendritic cells take up antigens from apoptotic neutrophils and serve as APC for T-cells. (5) Direct antigen presentation. ... T-cell activation by neutrophils is attained by (4) indirect antigen presentation. ...

https://www.immunopaedia.org.za/online-courses/previous-iuis-courses/immuno-ethiopia/neutrophils/neutrophil_tcells/

Segmented neutrophils number. English Text: Segmented neutrophils number. Target: Both males and females 1 YEARS - 150 YEARS. ... LBXNEPCT - Segmented neutrophils percent (%). Variable Name: LBXNEPCT. SAS Label: Segmented neutrophils percent (%). English ... Segmented neutrophils percent (%). Target: Both males and females 1 YEARS - 150 YEARS. Code or Value. Value Description. Count ... LBDNENO - Segmented neutrophils number. Variable Name: LBDNENO. SAS Label: ...

https://wwwn.cdc.gov/Nchs/Nhanes/1999-2000/LAB25.htm

Patrice E. Poubelle (Université Laval), co-chair Sylvain G. Bourgoin (Université Laval), treasurer ...

https://theneutrophil.com/zn2018/zn2018-organization/

Example ActivityDefinition: Neutrophils in blood ActivityDefinition. Generated Narrative. url: https://rarecare.world/fhir/ ...

http://fhir.rarecare.world/ActivityDefinition-act-neutrophils-in-blood.html

CHAGAS JUNIOR, Otacílio Luiz et al. Therapeutic laser and inflammatory cells - part 2: neutrophils. Rev. cir. traumatol. buco- ...

http://revodonto.bvsalud.org/scielo.php?script=sci_abstract&pid=S1808-52102013000300015&lng=pt&nrm=iso&tlng=en

The outcome of this study is expected to progress fundamental biology of neutrophils, increase our understanding of neutrophil ... Transcriptional Regulation of Neutrophil Differentiation and Function During Inflammation. Journal of Leukocyte Biology. 2020, ... IFN-lambda resolves inflammation via suppression of neutrophil infiltration and IL-1b-production. Journal of Experimental ... Neutrophils, inflammation, transcriptional regulators, genomics, mouse models, clinical samples. TRAINING OPPORTUNITIES. The ...

https://www.ndorms.ox.ac.uk/graduate-courses/kennedy-trust-prize-studentships/kennedy-trust-non-clinical-studentships/molecular-regulation-of-neutrophil-responses-in-inflammation

A skull bone marrow niche for antitumour neutrophils in glioblastoma A preprint by Lad et al. shows that tumour-associated ... neutrophils in glioblastoma originate from skull bone marrow and acquire an antigen-presenting cell phenotype intratumorally in ...

https://www.nature.com/nri/?type=progress&year=2008&error=cookies_not_supported&code=1b714b39-9263-4c8c-b16f-cdc60dda7396

Address : P.O. Box 15770 Flat No. 1, Bldg. No. 50, Road No. 2901, 329 Salmaniya - Bahrain ...

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Like the primitive macrophages, all primitive and larval neutrophils express PU.1 and L-plastin and they are highly attracted ... By 2 days after fertilization, these neutrophils have become the major leukocyte type found wandering in the epidermis and ... We were surprised to find that the differentiation of these primitive neutrophils occurs only after primitive myeloid ... Like the primitive macrophages, all primitive and larval neutrophils express PU.1 and L-plastin and they are highly attracted ...

https://hal-pasteur.archives-ouvertes.fr/pasteur-02558365v1

In addition, we quantified neutrophil elastase (ELISA) and net proteinase activity (substrate assay) in BALF. (dovepress.com)
We observed no corresponding correlations for neutrophil elastase, net proteinase or gelatinase activity. (dovepress.com)
Lee Biosolutions is the leading producer of human neutrophil Elastase (ELA2) for clinical research, life science and diagnostic manufacturing uses. (leebio.com)
The neutrophil form of elastase is 218 amino acids long, with two asparagine-linked carbohydrate chains. (leebio.com)
Current studies show that both Cathepsin G and Neutrophil Elastase are key enzymes for tissue injury caused by activated neutrophils, such as occurs in Acute Lung injury. (leebio.com)
One study with C57BL/6 mice demonstrated that the interaction of L. major-infected macrophages with dying neutrophils induced parasite destruction mediated by neutrophil elastase and tumour necrosis factor-α production from neutrophils [5]. (who.int)
NET-mediated osteoclastogenesis appears to depend on Toll-like receptor 4 signalling and NET-associated proteins including histones and neutrophil elastase. (bmj.com)

This amino acid has been shown to play a role in lymphocyte proliferation, cytokine production by lymphocytes and macrophages and phagocytosis and superoxide production by macrophages and neutrophils. (who.int)
Lymphocytes, macrophages and neutrophils play an important role in the immune and inflammatory response. (who.int)
The metabolic fate of glutamine in lymphocytes, macrophages and neutrophils will be discussed in the present paper. (who.int)
For instance, the tumor microenvironment modulates the immune response by selectively attracting and repolarizing immune cells (e.g. macrophages and neutrophils) from an anti-tumorigenic to a pro-tumorigenic phenotype ( 2 , 3 ). (frontiersin.org)

The three best described defense mechanisms of neutrophils are phagocytosis (engulfment of pathogenic microorganisms and subsequent destruction in phagosomes), degranulation (the release of antimicrobial proteins from granules to the extracellular space) and the formation of neutrophil extracellular traps (NETs). (elifesciences.org)
Carbamylation is a posttranslational modification linked to increased bone erosion in RA and we previously showed that carbamylation is present in RA neutrophil extracellular traps (NETs). (bmj.com)

The neutrophil-related cytokines IL-36α, -β and -γ were quantified (ELISA) along with IL-6, IL-8, INF-γ and CXCL10 (U-Plex ® ) in plasma and cell-free BAL fluid (BALF). (dovepress.com)

Neutrophils are important innate immune cells that tackle invading pathogens with different effector mechanisms. (elifesciences.org)
NETs are chromatin structures studded with antimicrobial proteins derived mostly from neutrophil granules, which can trap pathogens ( Papayannopoulos, 2018 ). (elifesciences.org)

In homeostatic conditions, up to 2 × 10 11 neutrophils enter the blood stream per day and patrol the host's body until they sense signs of infection, which triggers them to leave the blood stream and migrate to the inflammatory site where they ensure pathogen removal. (elifesciences.org)

Description: A sandwich quantitative ELISA assay kit for detection of Human Defensin Alpha 1, Neutrophil (DEFa1) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (lipidx.org)
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Mouse Defensin Alpha 1, Neutrophil (DEFa1) in serum, plasma, tissue homogenates and other biological fluids. (lipidx.org)
Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Mouse Defensin Alpha 1, Neutrophil (DEFa1) in samples from serum, plasma, tissue homogenates and other biological fluids with no significant corss-reactivity with analogues from other species. (lipidx.org)

One of these differentiation programs, called granulopoiesis, leads to the development of granulocytes - basophils, eosinophils and neutrophils. (elifesciences.org)

Large numbers of immature forms of neutrophils, called neutrophilic band cells, are produced by the bone marrow when the demand is high. (medlineplus.gov)
Neutrophils, also known as neutrophilic polymorphonuclear leukocytes, are the major class of white blood cell in human peripheral blood. (leebio.com)

Polymorphonuclear (PMN) neutrophils have been reported to have a crucial role in the destruction of the Leishmania major parasites at an early stage of infection [2,3]. (who.int)

Microscope images confirmed that neutrophils appeared to have an important role in leishmania elimination through phagocytosis of amastigotes in the later stages of the disease process. (who.int)

ABSTRACT Neutrophils are always present in the cytomorphologic process of leishmaniasis but their role is still not fully understood. (who.int)
article{18081955-679d-4f8b-aa8b-27b69763024d, abstract = {{We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ratio of GTP:GTP + GDP recovered on RhoA and translocation of RhoA to a membrane fraction. (lu.se)

Description: A sandwich ELISA kit for detection of Neutrophil Activating Protein 3 from Mouse in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (novosides.eu)

In smokers with COPD, altered glucose homeostasis is associated with local and systemic signs of increased neutrophil mobilization, but not with local proteinases. (dovepress.com)

Flow cytometric profiling of whole lung lavage (WLL) cells revealed that neutrophil recruitment was the greatest at day 1 and declined to 36.6% of that level in MWCNT- and 16.8% in C60F-treated mice by day 7, and to basal levels by day 28, suggesting a rapid initiation phase and an extended resolution phase. (cdc.gov)

Under homeostatic conditions, NET formation occurs in mature, circulating neutrophils and therefore we propose that specific cues during neutrophil differentiation shape their ability to form NETs. (elifesciences.org)
We were surprised to find that the differentiation of these primitive neutrophils occurs only after primitive myeloid progenitors have dispersed in the tissues. (archives-ouvertes.fr)

However, the mechanisms by which neutrophils participate in bone destruction remain unclear. (bmj.com)

Both ENMs stimulated acute inflammation, predominated by neutrophils, in the lung at day 1, which transitioned to histiocytic inflammation by day 7. (cdc.gov)

Neutrophils are a type of white blood cell that is responsible for much of the body's protection against infection. (medlineplus.gov)

Here, we show a critical role for linker histone H1 on the differentiation and function of neutrophils using a genome-wide CRISPR/Cas9 screen in the human cell line PLB-985. (elifesciences.org)
Loss of H1.2 and H1.4 induced an eosinophil-like transcriptional program, thereby negatively regulating the differentiation into the neutrophil lineage. (elifesciences.org)
Importantly, H1 subtypes also affect neutrophil differentiation and the eosinophil-directed bias of murine bone marrow stem cells, demonstrating an unexpected subtype-specific role for H1 in granulopoiesis. (elifesciences.org)

Given that these morbidities all display increased neutrophil mobilization, the current study aimed to address whether glucose homeostasis relates to signs of neutrophil mobilization in COPD. (dovepress.com)
The LTS+COPD group had lower fasting glucose, greater change in glucose during OGTT and higher neutrophil concentrations in BAL and blood compared with HNS. (dovepress.com)
Fasting glucose correlated in a positive manner with blood neutrophil concentration, forced expiratory volume in 1 second/forced vital capacity ratio (FEV 1 /FVC) and FEV 1 (% of predicted) in LTS+COPD. (dovepress.com)

Strikingly, we reveal that IFN-Î³ is expressed primarily by hepatic neutrophils , not by conventional immune cells with known IFN-Î³-producing capability, e.g. (bvsalud.org)

Neutrophils are produced in the bone marrow and released into the bloodstream to travel to wherever they are needed. (medlineplus.gov)
Objective Neutrophil infiltration into the synovial joint is a hallmark of rheumatoid arthritis (RA), a disease characterised by progressive bone erosion. (bmj.com)

The Absolute Neutrophil Count (ANC) is a calculated parameter based on the total number of white blood cells, the percentage of neutrophils, and the percentage of band cells in a patient's blood sample at a given time. (medscape.com)
Positivity for multiple IAs showed the lowest counts in white blood cells and neutrophils in boys and red blood cells, hemoglobin, and hematocrit in girls. (arctichealth.org)
We conclude that the reduction in neutrophils and red blood cells in children with multiple IAs and HLA-DR3-DQ2/DR4-DQ8 genotype may signal a sex-dependent islet autoimmunity detected in longitudinal CBCs. (arctichealth.org)
The use of Neutrophils from FERMT3 patients elucidated the requirement of kindlen3-CD18 interaction for synapse formation and trogocytosis of antibody opsinized SIRPa-CD47 checkpoint disruped cancer cells in vitro. (ancell.com)
Dr. Vora] Ted, it's a less common bacteria, which is in the category of what we call Gram- negative bacteria, and it is kind of rather unique because it likes to stay inside a cell and infect the defender cells, which are the neutrophils. (cdc.gov)

After the repetitive exposure, the older mice also had higher numbers of neutrophils in their BAL fluid. (cdc.gov)

A recent study from our laboratory has shown that neutrophils also utilize glutamine at high rates (6). (who.int)

In this study, the molecular mechanism behind the effectiveness of this combination therapy is investigated in human neutrophils. (springer.com)
Human neutrophils were preincubated with salmeterol or FP or the combination. (springer.com)
An efficient neutrophil response is crucial for human antimicrobial defense and, correspondingly, neutropenia is associated with severe infections ( Klein, 2011 ). (elifesciences.org)
We found that engagement of beta (2) integrins on human neutrophils induced activation of RhoA, as indicated by the increased ratio of GTP:GTP + GDP recovered on RhoA and translocation of RhoA to a membrane fraction. (lu.se)
This controlled opening and degradation was further carried out in vitro with human neutrophils. (cdc.gov)

Neutrophils also appear to play a major role in the development of protective immunity [5,6]. (who.int)
little has been mentioned about the role of neutrophils in the later stages of cutaneous leishmaniasis. (who.int)

The white blood cell and neutrophil counts were reduced in children with IAs, primarily in boys. (arctichealth.org)

Neutrophils were quantified in blood and bronchoalveolar lavage samples (BAL). (dovepress.com)
In this group, the concentration of IL-36α in BALF correlated in a negative manner with fasting glucose, blood neutrophil concentration and FEV 1 , while the CXCL10 concentration in BALF correlated in a negative manner with glucose at the end of OGTT (120 min). (dovepress.com)
Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish TEDDY Children at Increased Risk for Type 1 Diabetes. (arctichealth.org)

Neutrophils constitute 60% of the circulating leukocytes. (who.int)
Neutrophils are the most abundant leukocytes in humans. (elifesciences.org)

Cigarette smoke medium (CSM) induces an increased expression of CXC receptors and the production of ROS that may explain the strong production of IL-8 by neutrophils. (springer.com)
This leads eventually to suppression of both the NF-κB and MAPK pathways and, hence, to less IL-8 production by the neutrophil. (springer.com)

Neutrophils exacerbate acetaminophen-induced liver injury by producing cytotoxic interferon-Î³. (bvsalud.org)

By 2 days after fertilization, these neutrophils have become the major leukocyte type found wandering in the epidermis and mesenchyme. (archives-ouvertes.fr)

Recently, we have found that neutrophils also utilize glutamine. (who.int)

It kind of subverts the system of neutrophils and takes it over and prevents it from dying and just multiplies. (cdc.gov)

Notably, we observed a significant enrichment in transcripts involved in immune response pathways especially those contributing to neutrophil (IL8) and T-cell mediated immunity (BCL6, and CD81). (frontiersin.org)

undertaken from July 15th, 2017 to March 15th, 2018.The multicentrique de cohorte prospective a inclus des Glasgow Coma Scale helped to determine the severety of the patients consécutifs admis en phase aiguë d AVC, disease at admission. (who.int)

Anatomy32

Organisms8

Diseases28

Chemicals and Drugs134

Analytical, Diagnostic and Therapeutic Techniques and Equipment18

Phenomena and Processes34

Disciplines and Occupations1

Technology, Industry, Agriculture1

Information Science3

GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. (1/19639)

Interaction of inflammatory cells and oral microorganisms. II. Modulation of rabbit polymorphonuclear leukocyte hydrolase release by polysaccharides in response to Streptococcus mutans and Streptococcus sanguis. (2/19639)

Interaction of inflammatory cells and oral microorganisms. III. Modulation of rabbit polymorphonuclear leukocyte hydrolase release response to Actinomyces viscosus and Streptococcus mutans by immunoglobulins and complement. (3/19639)

Lung weight parallels disease severity in experimental coccidioidomycosis. (4/19639)

Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils. (5/19639)

Characterization and partial purification of a novel neutrophil membrane-associated kinase capable of phosphorylating the respiratory burst component p47phox. (6/19639)

Non-serum-dependent chemotactic factors produced by Candida albicans stimulate chemotaxis by binding to the formyl peptide receptor on neutrophils and to an unknown receptor on macrophages. (7/19639)

Role of the extracellular signal-regulated protein kinase cascade in human neutrophil killing of Staphylococcus aureus and Candida albicans and in migration. (8/19639)

Neutrophils

Neutrophil Infiltration

N-Formylmethionine Leucyl-Phenylalanine

Chemotaxis, Leukocyte

Peroxidase

Antigens, CD18

Phagocytosis

Superoxides

Chemotactic Factors

Macrophage-1 Antigen

Interleukin-8

Leukotriene B4

Leukocyte Count

Cell Adhesion

Pancreatic Elastase

Cathepsin G

Chemokine CXCL1

Receptors, Interleukin-8B

Zymosan

Complement C5a

Inflammation

NADPH Oxidase

Cells, Cultured

Chemokine CXCL2

Granulomatous Disease, Chronic

Receptors, Formyl Peptide

Cell Movement

Cytoplasmic Granules

Lipopolysaccharides

L-Selectin

Lung

Tetradecanoylphorbol Acetate

Cell Degranulation

Myeloblastin

Luminescent Measurements

Bronchoalveolar Lavage Fluid

alpha-Defensins

Platelet Activating Factor

Mice, Knockout

Granulocyte Colony-Stimulating Factor

Leukocytes

Tumor Necrosis Factor-alpha

Blood Bactericidal Activity

Antigens, CD11b

Receptors, Interleukin-8A

Receptors, IgG

HL-60 Cells

Flow Cytometry

Chemokines

Lactoferrin

Lipocalins

Granulocyte-Macrophage Colony-Stimulating Factor

Neutropenia

Leukocyte Disorders

Cytochalasin B

Chemotaxis

Hypochlorous Acid

Chemokines, CXC

Cytokines

P-Selectin

Eosinophils

Monocytes

Opsonin Proteins

Macrophages

Apoptosis

Granulocytes

Cell Adhesion Molecules

NADH, NADPH Oxidoreductases

Reactive Oxygen Species

Antigens, CD11

Antigens, CD

Disease Models, Animal

Signal Transduction

Intercellular Adhesion Molecule-1

Time Factors

Acute-Phase Proteins

Transendothelial and Transepithelial Migration

Antibodies, Monoclonal

Leukocyte Rolling

Complement C5