The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).
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 large protein complex which acts as a signaling adaptor protein that allows communication between the various regulatory and functional components of GENETIC TRANSCRIPTION including DNA POLYMERASE II; GENERAL TRANSCRIPTION FACTORS; and TRANSCRIPTION FACTORS that are bound to upstream ENHANCER ELEMENTS. The mediator complex was originally studied in YEAST where at least 21 subunits were identified. Many of the yeast subunits are homologs to proteins in higher organisms that are found associated with specific nuclear receptors such as THYROID HORMONE RECEPTORS and VITAMIN D RECEPTORS.
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.
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.
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.
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.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
Substances that reduce or suppress INFLAMMATION.
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.
Infection of the lung often accompanied by inflammation.
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.
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.)
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.
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)
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.
Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury.
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 plasma protein that circulates in increased amounts during inflammation and after tissue damage.
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.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
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.
Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.
An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.
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 albumin obtained from the white of eggs. It is a member of the serpin superfamily.
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
A water-soluble extractive mixture of sulfated polysaccharides from RED ALGAE. Chief sources are the Irish moss CHONDRUS CRISPUS (Carrageen), and Gigartina stellata. It is used as a stabilizer, for suspending COCOA in chocolate manufacture, and to clarify BEVERAGES.
Any inflammation of the skin.
A form of hypersensitivity affecting the respiratory tract. It includes ASTHMA and RHINITIS, ALLERGIC, SEASONAL.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
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.
Tendency of the smooth muscle of the tracheobronchial tree to contract more intensely in response to a given stimulus than it does in the response seen in normal individuals. This condition is present in virtually all symptomatic patients with asthma. The most prominent manifestation of this smooth muscle contraction is a decrease in airway caliber that can be readily measured in the pulmonary function laboratory.
Elements of limited time intervals, contributing to particular results or situations.
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 chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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.
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
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
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.
Established cell cultures that have the potential to propagate indefinitely.
Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Antigen-type substances that produce immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
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.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
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.
An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.
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.
Granulated cells that are found in almost all tissues, most abundantly in the skin and the gastrointestinal tract. Like the BASOPHILS, mast cells contain large amounts of HISTAMINE and HEPARIN. Unlike basophils, mast cells normally remain in the tissues and do not circulate in the blood. Mast cells, derived from the bone marrow stem cells, are regulated by the STEM CELL FACTOR.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
Chronic, non-specific inflammation of the GASTROINTESTINAL TRACT. Etiology may be genetic or environmental. This term includes CROHN DISEASE and ULCERATIVE COLITIS.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Disease having a short and relatively severe course.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.
A pattern recognition receptor that interacts with LYMPHOCYTE ANTIGEN 96 and LIPOPOLYSACCHARIDES. It mediates cellular responses to GRAM-NEGATIVE BACTERIA.
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
Long-chain polymer of glucose containing 17-20% sulfur. It has been used as an anticoagulant and also has been shown to inhibit the binding of HIV-1 to CD4-POSITIVE T-LYMPHOCYTES. It is commonly used as both an experimental and clinical laboratory reagent and has been investigated for use as an antiviral agent, in the treatment of hypolipidemia, and for the prevention of free radical damage, among other applications.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
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.
The number of WHITE BLOOD CELLS per unit volume in venous BLOOD. A differential leukocyte count measures the relative numbers of the different types of white cells.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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 concrete oleoresin obtained from Pinus palustris Mill. (Pinaceae) and other species of Pinus. It contains a volatile oil, to which its properties are due, and to which form it is generally used. (Dorland, 28th ed) Turpentine is used as a solvent and an experimental irritant in biomedical research. Turpentine toxicity is of medical interest.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Inflammation of any segment of the ILEUM and the ILEOCECAL VALVE.
The mucous membrane lining the RESPIRATORY TRACT, including the NASAL CAVITY; the LARYNX; the TRACHEA; and the BRONCHI tree. The respiratory mucosa consists of various types of epithelial cells ranging from ciliated columnar to simple squamous, mucous GOBLET CELLS, and glands containing both mucous and serous cells.
A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.
The larger air passages of the lungs arising from the terminal bifurcation of the TRACHEA. They include the largest two primary bronchi which branch out into secondary bronchi, and tertiary bronchi which extend into BRONCHIOLES and PULMONARY ALVEOLI.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
A reagent that is used to neutralize peptide terminal amino groups.
A mediator complex subunit that is believed to play a key role in the coactivation of nuclear receptor-activated transcription by the mediator complex. It interacts with a variety of nuclear receptors including RETINOIC ACID RECEPTORS; THYROID HORMONE RECEPTORS; VITAMIN D RECEPTORS; PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS; ESTROGEN RECEPTORS; and GLUCOCORTICOID RECEPTORS.
A negative 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 class of compounds named after and generally derived from C20 fatty acids (EICOSANOIC ACIDS) that includes PROSTAGLANDINS; LEUKOTRIENES; THROMBOXANES, and HYDROXYEICOSATETRAENOIC ACIDS. They have hormone-like effects mediated by specialized receptors (RECEPTORS, EICOSANOID).
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
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.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system.
Abnormal increase of EOSINOPHILS in the blood, tissues or organs.
The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)
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.
INFLAMMATION of PLEURA, the lining of the LUNG. When PARIETAL PLEURA is involved, there is pleuritic CHEST PAIN.
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.
A cytokine synthesized by T-LYMPHOCYTES that produces proliferation, immunoglobulin isotype switching, and immunoglobulin production by immature B-LYMPHOCYTES. It appears to play a role in regulating inflammatory and immune responses.
Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. (Dorland, 27th ed)
The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.
Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.
A CXC chemokine that is synthesized by activated MONOCYTES and NEUTROPHILS. It has specificity for CXCR2 RECEPTORS.
An antigen solution emulsified in mineral oil. The complete form is made up of killed, dried mycobacteria, usually M. tuberculosis, suspended in the oil phase. It is effective in stimulating cell-mediated immunity (IMMUNITY, CELLULAR) and potentiates the production of certain IMMUNOGLOBULINS in some animals. The incomplete form does not contain mycobacteria.
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.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
Inflammation of any part of the KIDNEY.
Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)
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.
The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes SYNOVIAL FLUID.
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
Inflammation of the large airways in the lung including any part of the BRONCHI, from the PRIMARY BRONCHI to the TERTIARY BRONCHI.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Adherence of cells to surfaces or to other cells.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
A CXC chemokine with specificity for CXCR2 RECEPTORS. It has growth factor activities and is implicated as a oncogenic factor in several tumor types.
A condition characterized by infiltration of the lung with EOSINOPHILS due to inflammation or other disease processes. Major eosinophilic lung diseases are the eosinophilic pneumonias caused by infections, allergens, or toxic agents.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
Proteins prepared by recombinant DNA technology.
A systemic inflammatory response to a variety of clinical insults, characterized by two or more of the following conditions: (1) fever >38 degrees C or HYPOTHERMIA 90 beat/minute; (3) tachypnea >24 breaths/minute; (4) LEUKOCYTOSIS >12,000 cells/cubic mm or 10% immature forms. While usually related to infection, SIRS can also be associated with noninfectious insults such as TRAUMA; BURNS; or PANCREATITIS. If infection is involved, a patient with SIRS is said to have SEPSIS.
Mice bearing mutant genes which are phenotypically expressed in the animals.
Methods used for detecting the amplified DNA products from the polymerase chain reaction as they accumulate instead of at the end of the reaction.
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.
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.
An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Also known as articulations, these are points of connection between the ends of certain separate bones, or where the borders of other bones are juxtaposed.
Inflammation of any segment of the SMALL INTESTINE.
A cytokine that promotes differentiation and activation of EOSINOPHILS. It also triggers activated B-LYMPHOCYTES to differentiate into IMMUNOGLOBULIN-secreting cells.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonized particles, immune complexes, and chemotactic factors, bind to specific cell-surface receptors on the neutrophil.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A condition characterized by the presence of ENDOTOXINS in the blood. On lysis, the outer cell wall of gram-negative bacteria enters the systemic circulation and initiates a pathophysiologic cascade of pro-inflammatory mediators.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
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.
Restoration of integrity to traumatized tissue.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
A family of pattern recognition receptors characterized by an extracellular leucine-rich domain and a cytoplasmic domain that share homology with the INTERLEUKIN 1 RECEPTOR and the DROSOPHILA toll protein. Following pathogen recognition, toll-like receptors recruit and activate a variety of SIGNAL TRANSDUCING ADAPTOR PROTEINS.
An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A 24-kDa HMGB protein that binds to and distorts the minor grove of DNA.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells.
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
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.
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.
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.
An interleukin-1 subtype that occurs as a membrane-bound pro-protein form that is cleaved by proteases to form a secreted mature form. Unlike INTERLEUKIN-1BETA both membrane-bound and secreted forms of interleukin-1alpha are biologically active.
Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.
A pattern recognition receptor that forms heterodimers with other TOLL-LIKE RECEPTORS. It interacts with multiple ligands including PEPTIDOGLYCAN, bacterial LIPOPROTEINS, lipoarabinomannan, and a variety of PORINS.
Forceful administration into the peritoneal cavity of liquid medication, nutrient, or other fluid through a hollow needle piercing the abdominal wall.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
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.
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.
The structural changes in the number, mass, size and/or composition of the airway tissues.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Inflammation of the cornea.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
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).
A cell line derived from cultured tumor cells.
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.
INFLAMMATION of the placental membranes (CHORION; AMNION) and connected tissues such as fetal BLOOD VESSELS and UMBILICAL CORD. It is often associated with intrauterine ascending infections during PREGNANCY.
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 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.
Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.
Pathological processes involving any part of the LUNG.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
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.

Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (1/6604)

Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1-3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1beta mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor-BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells.  (+info)

Dephosphorylation of the catenins p120 and p100 in endothelial cells in response to inflammatory stimuli. (2/6604)

Inflammatory mediators such as histamine and thrombin increase the tight-junction permeability of endothelial cells. Tight-junction permeability may be independently controlled, but is dependent on the adherens junction, where adhesion is achieved through homotypic interaction of cadherins, which in turn are associated with cytoplasmic proteins, the catenins. p120, also termed p120(cas)/p120(ctn), and its splice variant, p100, are catenins. p120, originally discovered as a substrate of the tyrosine kinase Src, is also a target for a protein kinase C-stimulated pathway in epithelial cells, causing its serine/threonine dephosphorylation. The present study shows that pharmacological activation of protein kinase C stimulated a similar pathway in endothelial cells. Activation of receptors for agents such as histamine (H1), thrombin and lysophosphatidic acid in the endothelial cells also caused serine/threonine dephosphorylation of p120 and p100, suggesting physiological relevance. However, protein kinase C inhibitors, although blocking the effect of pharmacological activation of protein kinase C, did not block the effects due to receptor activation. Calcium mobilization and the myosin-light-chain-kinase pathway do not participate in p120/p100 signalling. In conclusion, endothelial cells possess protein kinase C-dependent and -independent pathways regulating p120/p100 serine/threonine phosphorylation. These data describe a new connection between inflammatory agents, receptor-stimulated signalling and pathways potentially influencing intercellular adhesion in endothelial cells.  (+info)

CD40 signaling of monocyte inflammatory cytokine synthesis through an ERK1/2-dependent pathway. A target of interleukin (il)-4 and il-10 anti-inflammatory action. (3/6604)

Ligation of CD40 on monocytes through its interaction with CD40 ligand (CD154) present on activated T helper cells, results in activation of monocyte inflammatory cytokine synthesis and rescue of monocytes from apoptosis induced through serum deprivation. Both of these consequences of CD40 stimulation have been shown to be dependent on the induction of protein tyrosine kinase activity. CD40-mediated activation of protein tyrosine kinase activity and subsequent inflammatory cytokine production are abrogated by treatment of monocytes with the T helper type 2 cytokines interleukin 4 (IL-4) and interleukin 10 (IL-10). In the current study we demonstrate that stimulation of monocytes through CD40 resulted in the phosphorylation and activation of the extracellular signal-regulated kinases 1 and 2 (ERK1/2) mitogen-activated protein kinases, whereas phosphorylation of mitogen-activated protein kinases family members p38 and c-Jun N-terminal kinase was not observed in response to this stimuli over the time course examined. PD98059, an inhibitor of the upstream activator of ERK1/2, the MAP/ERK kinase MEK1/2, suppressed IL-1beta and tumor necrosis factor-alpha production in a dose-dependent fashion. Pretreatment of monocytes with IL-4 and IL-10 inhibited CD40-mediated activation of ERK1/2 kinase activity when used individually, and are enhanced in effectiveness when used in combination. Together, the data demonstrate that CD40-mediated induction of IL-1beta and tumor necrosis factor-alpha synthesis is dependent on a MEK/ERK pathway which is obstructed by signals generated through the action of IL-4 and IL-10.  (+info)

The vitronectin receptor and its associated CD47 molecule mediates proinflammatory cytokine synthesis in human monocytes by interaction with soluble CD23. (4/6604)

The vitronectin receptor, alphavbeta3 integrin, plays an important role in tumor cell invasion, angiogenesis, and phagocytosis of apoptotic cells. CD47, a member of the multispan transmembrane receptor family, physically and functionally associates with vitronectin receptor (VnR). Although vitronectin (Vn) is not a ligand of CD47, anti-CD47 and beta3 mAbs suppress Vn, but not fibronectin (Fn) binding and function. Here, we show that anti-CD47, anti-beta3 mAb and Vn, but not Fn, inhibit sCD23-mediated proinflammatory function (TNF-alpha, IL-12, and IFN-gamma release). Surprisingly, anti-CD47 and beta3 mAbs do not block sCD23 binding to alphav+beta3+ T cell lines, whereas Vn and an alphav mAb (clone AMF7) do inhibit sCD23 binding, suggesting the VnR complex may be a functional receptor for sCD23. sCD23 directly binds alphav+beta3+/CD47(-) cell lines, but coexpression of CD47 increases binding. Moreover, sCD23 binds purified alphav protein and a single human alphav chain CHO transfectant. We conclude that the VnR and its associated CD47 molecule may function as a novel receptor for sCD23 to mediate its proinflammatory activity and, as such, may be involved in the inflammatory process of the immune response.  (+info)

The effects of inflammation and inflammatory mediators on nociceptive behaviour induced by ATP analogues in the rat. (5/6604)

1. We have studied the behavioural effects of intraplantar injections of adenosine 5'-triphosphate (ATP) and related compounds in freely moving rats and investigated whether these nociceptive effects are augmented in the presence of inflammatory mediators. 2. We find that in normal animals ATP and analogues produce dose-dependent nocifensive behaviour (seen as bursts of elevation of the treated hindpaw), and localized thermal hyperalgesia. The rank order of potency was: alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-methylene ATP) > 2-methylthioadenosine triphosphate (2-methylthio ATP) > ATP. After neonatal treatment with capsaicin, to destroy small calibre primary sensory neurones, nocifensive behaviour was largely absent. 3. The effects of ATP analogues were assessed in three models of peripheral sensitization: 2 h after dilute intraplantar carrageenan (0.25% w v(-1)); 24 h after irradiation of the hindpaw with ultraviolet (U.V.) B; immediately following prostaglandin E2 (PGE2) treatment. In all models the effect of alpha,beta-methylene ATP was greatly augmented. After carrageenan, significant hindpaw-lifting behaviour activity was induced by injection of only 0.05 nmol of alpha,beta-methylene ATP, some 100 times less than necessary in normal skin. 4. Our data suggest that it is much more likely that endogenous levels of ATP will reach levels capable of exciting nociceptors in inflamed versus normal skin. Our data also suggest the involvement of P2X3 receptor subunits in ATP-induced nociception.  (+info)

Airway inflammatory response to ozone in subjects with different asthma severity. (6/6604)

The aim of this study was to evaluate whether ozone exposure induces a similar airway inflammatory response in subjects with different degrees of asthma severity. Two groups of asthmatic subjects were studied: seven with intermittent mild asthma not requiring regular treatment (group A); and seven with persistent mild asthma requiring regular treatment with inhaled corticosteroids and long-acting beta2-agonists (group B). All subjects were exposed, in a randomized cross-over design, to air or O3 (0.26 parts per million (ppm) for 2 h with intermittent exercise); subjects in group B withdrew from regular treatment 72 h before each exposure. Before the exposure, and 1 and 2 h after the beginning of the exposure they performed a pulmonary function test, and a questionnaire was completed to obtain a total symptom score (TSS). Six hours after the end of the exposure, hypertonic saline (HS) sputum induction was conducted. Sputum cell percentages, eosinophil cationic protein (ECP) and interleukin (IL)-8 concentrations in the sputum supernatant were measured. TSS significantly increased and forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) significantly decreased after O3 exposure in comparison with air exposure in group A, whereas no changes were observed in group B except for a significant decrement of FEV1 2 h after the beginning of O3 exposure. Sputum neutrophil percentage was significantly higher after O3 exposure than after air exposure in both groups (Group A: 70.2% (28-87) versus 26.6% (8.6-73.2); Group B: 62.1% (25-82.4) versus 27.9% (14.4-54)). IL-8 was higher in sputum supernatant collected 6 h after O3 exposure than after air, only in group A. No change due to O3 has been found in sputum eosinophil percentage and ECP concentration in both groups. In conclusion, the degree of airway response to a short-term exposure to ozone is different in subjects with asthma of different severity. The available data do not allow elucidation of whether this difference depends on the severity of the disease or on the regular anti-inflammatory treatment.  (+info)

Cytokines and inflammatory mediators do not indicate acute infection in cystic fibrosis. (7/6604)

Various treatment regimens and difficulties with research design are encountered with cystic fibrosis (CF) because no standard diagnostic criteria exist for defining acute respiratory exacerbations. This study evaluated the role of serial monitoring of concentrations of selected cytokines and inflammatory mediators in serum and sputum as predictors of respiratory exacerbation, as useful outcome measures for CF, and to guide therapy. Interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-alpha), neutrophil elastase-alpha-1-protease inhibitor complex (NE complex), protein, and alpha-1-protease inhibitor (alpha-1-PI) were measured in serum and sputum collected from CF patients during respiratory exacerbations and periods of well-being. Levels of NE complex, protein, and alpha-1-PI in sputum rose during respiratory exacerbations and fell after institution of antibiotic therapy (P = 0.078, 0.001, and 0.002, respectively). Mean (+/- standard error of the mean) levels of IL-8 and TNF-alpha were extremely high in sputum (13,780 +/- 916 and 249.4 +/- 23.5 ng/liter, respectively) but did not change significantly with clinical deterioration of the patient (P > 0.23). IL-8 and TNF-alpha were generally undetectable in serum, and therefore these measures were unhelpful. Drop in forced expiratory volume in 1 s was the only clinical or laboratory parameter that was close to being a determinant of respiratory exacerbation (P = 0.055). This study provides evidence of intense immunological activity occurring continually within the lungs of adult CF patients. Measurement of cytokines and inflammatory mediators in CF sputum is not helpful for identifying acute respiratory exacerbations.  (+info)

Murine p38-delta mitogen-activated protein kinase, a developmentally regulated protein kinase that is activated by stress and proinflammatory cytokines. (8/6604)

The p38 mitogen-activated protein kinases (MAPK) play a crucial role in stress and inflammatory responses and are also involved in activation of the human immunodeficiency virus gene expression. We have isolated the murine cDNA clones encoding p38-delta MAPK, and we have localized the p38-delta gene to mouse chromosome 17A3-B and human chromosome 6p21.3. By using Northern and in situ hybridization, we have examined the expression of p38-delta in the mouse adult tissues and embryos. p38-delta was expressed primarily in the lung, testis, kidney, and gut epithelium in the adult tissues. Although p38-delta was expressed predominantly in the developing gut and the septum transversum in the mouse embryo at 9.5 days, its expression began to be expanded to many specific tissues in the 12.5-day embryo. At 15.5 days, p38-delta was expressed virtually in most developing epithelia in embryos, suggesting that p38-delta is a developmentally regulated MAPK. Interestingly, p38-delta and p38-alpha were similar serine/threonine kinases but differed in substrate specificity. Overall, p38-delta resembles p38-gamma, whereas p38-beta resembles p38-alpha. Moreover, p38-delta is activated by environmental stress, extracellular stimulants, and MAPK kinase-3, -4, -6, and -7, suggesting that p38-delta is a unique stress-responsive protein kinase.  (+info)

Blood-derived monocytes are found at sites of inflammation as well as in solid tumors and atherosclerotic arteries. They are an abundant source of inflammatory eicosanoids such as prostaglandin E2 (PGE2) and thromboxane A2, which are formed via arachidonic acid (AA) metabolism by cyclooxygenase-1/2 (COX-1/2). In vitro studies of inflammatory mediator production are conducted invariably in room air, which does not reflect the oxygen tensions found in monocyte-containing lesions, which are frequently hypoxic. In this work we examined the effects of hypoxia at levels reported in these lesions, on monocyte COX-2 expression, the related events that lead to eicosanoid synthesis, and relationships with tumor necrosis factor (TNF)-alpha synthesis. In fresh human monocytes exposed to hypoxia (1% O2), there was an increase in COX-2 protein compared with cells in normoxia, and this was attributable to increased transcription and mRNA stability. However, the synthesis of PGE2 and thromboxane A2 was reduced ...
Post-ischemic inflammation in the brain. Within 24 h after ischemic stroke onset, various inflammatory mediators are expressed in ischemic brain tissue. ICAM-
The research focus of the section molecular pharmacology concerns the role of glia cells (astrocytes and microglia) in psychatric and neurodegenerative diseases. The human brain hosts more glia cells than neurons and the importance of glia cells in all brain functions has been recognized in the last 10 years.. Our major scientific interest relates to the protective function of glia cells that are based on the release of inflammatory mediators (cytokines and chemokines). Since these inflammatory mediators are most likely also important in psychiatric diseases like Alzheimers disease, depression or schizophrenia the role of these mediators in vitro and in vivo are investigated.. The several molecular and biochemical research projects are performed in close collaboration with the section Psychopharmakotherapy and the neurochemical lab. ...
Effect of Potulacea L. on some Proinflammatory factors in Obese Adolescents , Effect of Potulacea L. on some Proinflammatory factors in Obese Adolescents , کتابخانه دیجیتال دانشگاه علوم پزشکی اصفهان
This project addresses possible biological mechanisms underlying the adverse human health effects associated with exposure to the respirable fine particulate matter present in air pollution (PM2.5). Epidemiological studies suggest that humans, especially those with chronic pulmonary or cardiovascular disease, are adversely affected by exposure to PM2.5 and animal toxicological studies have shown that PM2.5 introduced into the respiratory tract cause adverse health effects such as inflammation. In order to bridge the gap between human epidemiological and animal toxicological studies, this research will investigate the effects of PM2.5 upon human respiratory tract epithelial cells. The underlying hypothesis of this research is that respirable particulates carry as yet unidentified toxic environmental chemicals into the respiratory tract where they are deposited onto the epithelial cell lining and act to disrupt normal epithelial cell functions, resulting in inflammation. ...
TAK-242 (resatorvid), a small molecule specific inhibitor of Toll-like receptor (TLR) 4 signaling, inhibits the production of lipopolysaccharide-induced inflammatory mediators by binding to the intracellular domain of TLR4. Previously, Cys747 in TLR4 was identified as the binding site of TAK-242. However, the mechanism by which TAK-242 inhibits TLR4 signaling after binding to TLR4 remains unknown. The present study demonstrated, using coimmunoprecipitation, that TAK-242 interferes with protein-protein interactions between TLR4 and its adaptor molecules. Among ten different human TLRs, TAK-242 selectively bound to TLR4. The time course of the inhibitory effect of TAK-242 on inflammatory mediator production corresponded to that of the binding of TAK-242 to TLR4. TAK-242 inhibited the association of TLR4 with TIR domain-containing adaptor protein (TIRAP) or TRIF-related adaptor molecule (TRAM) in HEK293 cells overexpressing TLR4, MD-2 and TIRAP or TRAM, respectively. TAK-242 inhibited the ...
The humoral immune response, also known as the antibody-mediated immune response, targets pathogens circulating in extracellular fluids (lymph or the blood). It involves B-cells that recognize antigens of pathogens. The secretion of soluble antibodies by the antibody-secreting plasma cells causes the destruction of extracellular microorganisms, preventing the spread of intracellular infections. Immunization can be attained through this humoral response.. Every step of the humoral response can be monitored, offering multiple solutions to support antiviral therapies and vaccines discovery.. Vaccination and immunity are closley linked to inflammation. Cytokines, inflammatory pathways, and inflammatory mediators are the hallmarks of those processes. During infection, multiple pathways like NFKB, JAK-STAT and, MAP Kinase are activated to contribute to cell stimulation. IL-6, IL1β, TNFα and the different IFN (-γ, -α, -β), among others, can be at the origin of the activation of these pathways and ...
The p38 MAPK signaling pathway regulates expression of many inflammatory mediators at a posttranscriptional level via MK2-mediated stabilization of otherwise highly labile mRNAs (16, 22). At least some of these inflammatory mediators are also known to be posttranscriptionally controlled by TTP, a well-characterized mRNA destabilizing factor. The reasons for studying functional links between p38 MAPK and TTP are therefore clear, yet there remains controversy over whether TTP is a substrate of p38 MAPK itself, MK2, or both (8, 10, 15, 47, 67); whether or not such phosphorylation alters TTP function (52, 56) (T. Santalucia, M. Brook, E. Hitti, et al., unpublished); and whether or not it results in recruitment of 14-3-3 proteins (15, 52, 56). Several previous studies have been performed using cell types that express little or no endogenous TTP and in which overexpression of the protein may subvert the normal regulation of stability, localization, or function. With this in mind, here we performed ...
Type 1 diabetes (T1D) is an inflammatory disorder as is obesity. This thesis addresses inflammatory features in both conditions, with focus on inflammatory mediators and the role of adipose tissue (AT). The first part, specific aspects of immune tolerance in T1D,focuses on immune (dys) regulation and biomarkers for the immune responses ... read more elicited in T1D. Recognition of pan HLA-DR binding HSP-60 epitopes in paediatric new-onset T1D patients is studied and compared with longstanding T1D patients as well as healthy controls. Although HSP60 peptides induced low peptide-specific proliferative responses we detected some, mainly intracellular, peptide-specific cytokine production in T1D patients. Biomarkers for the remission period could not be identified. Next, we report our finding that autoreactive CD8 T cells, recognizing preproinsulin (PPI) peptides binding with very low affinity to HLA molecules, appear to escape thymic selection while numbers of PPI specific CD8 T cells are decreased ...
The care of the critically ill patient has become the point of convergence for substrate and energy metabolism, vital organ support, and cell biology. This article includes a brief review of normal metabolism and its endocrine regulation. The metabolic response to injury is reviewed with special attention to insulin resistance. The metabolic response to infection is considered in the light of rapidly emerging information on inflammatory mediators. Finally, brief attention is given to microcirculation and pericellular fluid as sites of metabolic regulation that have the potential for contributing to each of the three converging disciplines.
Inflammation not only occurs when we do something like twist an ankle or wrist or land wrong on a knee or elbow, it can also occur if we are unhealthy.. In a recent study, researchers found that overweight men are at greater risk of inflammation than men of the same age who are more fit. This was largely due to unfit men having a higher white blood cell count than healthier men. For women, inflammation drops when they lose weight. A different study found that obese women who lost more than 5% of their body weight had lower levels of inflammation markers.. While inflammation can help a body heal, it has a time and place. That means if we are unhealthy and causing our bodies to become inflamed regularly, we can be at risk for several types of cancer and even heart disease.. Perhaps most shocking, if inflammation is occurring so often that it becomes a part of your every day life, it can lead to hyperactive healing that can damage tissues and even result in chronic inflammation. If inflammation ...
Roth, I., Campbell, H., Rubio, C., Vennin, C., Wilson, M., Wiles, A., Williams, G., Woolley, A., Timpson, P., Berridge, M., Braithwaite, A., et al (2016). The (delta)133p53 isoform and its mouse analogue (delta)122p53 promote invasion and metastasis involving pro-inflammatory molecules interleukin-6 and CCL2. Oncogene, 35(38), 4981-4989. [More Information] ...
Inflammation is normally the bodys protective response to injury or destruction of tissue. Although many people consider it negative, inflammation can actually be a good sign.. Inflammation is adaptive and serves a purpose because it indicates that the body has detected a problem. But the chronic low-grade inflammation causes long-term damage to tissues and is believed to be major chronic illnesses.. Chronic inflammation damages tissues and organs and robs them of nutrients. It can be caused by some foods and is highly dangerous for your health. ...
If a cut on your skin swells up, turns purple, and hurts, these signs are indications of acute, or quick-lived, inflammation. Feeling hot or dropping operate may well be indications of inflammation from other damage to your body. Some inflammation that occurs in your bodys cells or tissues may well not have outward signs.. Inflammation is a ordinary element of the bodys protection to damage or infection, and, in this way, it is beneficial. But inflammation is detrimental when it occurs in healthful tissues or lasts as well very long. Regarded as continual inflammation, it may well persist for months or several years.. Inflammation may well result from a lot of components, this kind of as:. ...
If you have a condition such as muscle/joint aches, skin concerns, allergies, or something more serious - consider that inflammation may be the problem and your liver may need support!. There are two types of inflammation.. Acute Inflammation - this is a normal immune system response to injury or infection to promote healing.. Chronic inflammation - this occurs when the body is under constant stressors which may lead to a breakdown in the immune system.. So, how does the liver connect with this inflammation and why is it so important?. The liver is a filtering system but it also converts nutrients into active forms for our body to use. The liver has functions with blood sugar balance, hormone balance, clotting factors, allergies, and more. So, when the body is under stress, this can lead to inflammation and the liver cannot fully function. When the liver is unable to function, then all or many of those connections can go out of balance and the outcome may manifest as symptoms or illness.. What ...
Acute inflammation is a healthy part of your bodys defense system. You need it to manage injury, infection, and the healing process. On the other hand, excess, long-term, or chronic inflammation is a major cause of disease in the modern world.. Modern health science pays careful attention to signs that your body is in an inflammatory state. There are key mediators, or biomarkers, that you can find in the blood that accurately measure how well youre aging and whether or not youre developing the common diseases of the elderly.. Inflammation is not only linked to cancer and heart disease, but diabetes, arthritis, hypertension, autoimmune disease, and aging, itself.. These markers of inflammation and pro-inflammatory cytokines that can be found in your blood can really tell you a whole lot about your present and your future. They are:. ...
There are natural, healthy foods you can choose which may help reduce and even prevent inflammation. Inflammation is your bodys natural response to injury or infection. Chronic inflammation, also known as internal inflammation is a continuous, system-wide inflammation characterized by constant tearing down then healing of tissues and internal organs. Chronic inflammation may be triggered […]. ...
There are natural, healthy foods you can choose which may help reduce and even prevent inflammation. Inflammation is your bodys natural response to injury or infection. Chronic inflammation, also known as internal inflammation is a continuous, system-wide inflammation characterized by constant tearing down then healing of tissues and internal organs. Chronic inflammation may be triggered […]. ...
Our research line is made of three sublines, specialized in the investigation of brain pathologies, including cerebrovascular diseases, neurodegenerative diseases, and brain ageing.. ...
Inflammation…we are all familiar with this term! Inflammation, when it is as a result of an injury, is a healthy response. Its part of the healing process. Unfortunately, inflammation can also get out of control and become the cause of pain and suffering as it wont go away without intervention. Although younger people can suffer from it, it is generally an older persons problem. You only need to look around you to see the number of people obviously suffering. They are walking around hunched over, obviously in pain, and their movements are not as fluid as when they were younger. Now, these are the obvious signs…and painful ones. But there are other factors with regard to inflammation that are not only not obvious; they are completely silent with no indications of a problem. I am talking about inflammation in your arteries. ...
Inflammation is a protective response by the body towards cell injury. Cell injury may be due to; necrotic cells or tissue, the introduction of microbes (such as viruses or bacteria), toxins, hypoxia, etc. Inflammation is therefore the bodys way of attempting to remove the primary cause of inflammation and any damage that may have occurred as a result (Healing and repair). However if inflammation did not occur, then the body would be unable to deal with wounds and infections letting them go unchecked and progressively destroy the tissue. All injured organs would therefore be unable to regain function, eventually leading to mortality.. Inflammation is a complicated series of biological reactions, only taking place in vascularised tissue, simply however it works by attempting to remove, dilute or barricade the injurious/pathogenic agent or tissue. Its secondary role is to induce the healing and the repair of the damaged tissue. The result of this is an accumulation of leukocytes and fluid in the ...
Inflammation is the bodys natural response to infection and injury. While initial inflammation is necessary for healthy healing, prolonged inflammation can actually decrease the bodys immunity and prevent tissues from repairing. Here are some tips to reduce chronic inflammation without the need for over the counter medication.. ...
Inflammation, Breathing and Oxygen Lots of talk about inflammation these days. Inflammation is not a cause, it is a symptom. Acute or chronic. Acute is the warning and healing reaction. Chronic is the bad one. It will be interesting when we can scan for low grade chronic inflammation and then using medicine, or diet o
Inflammation can happen at any age, but does increase with age. Natural methods to reducing inflammation can support your health and help and prevent disease.
Inflammation is the bodys natural reaction against injury and infection. But chronic inflammation can contribute to the buildup of fatty plaque inside…
Written by: Kavata Kithome We talk a lot about inflammation here at Fitlife. This is because most people suffer from inflammation in some way, shape,(...)
Quantibody|sup|®|/sup| Human Inflammation Array 3 Kit. Detects 40 Human Inflammatory Factors. Suitable for all liquid sample types.
Thats why its important to eat a well-balanced diet that includes inflammation reducing foods.While reduce inflammation is part of that immune response
Inflammation is one of our nations leading cause of disease. Why is this? We explore what inflammation is and why so many of us struggle with it. ...
An overview of the cardiovascular and inflammation, introduction, the mechanism of inflammation in cardiovascular and clinical significance
You may be well-informed about health conditions linked to inflammation, what exactly is the deal with it? Watch this video to learn more how inflammation affects your body.
Youve probably heard me mention the word inflammation before or heard it from some other source since its a buzz word in the health and wellness industry lately. Lets take a look at inflammation again from the ground up.
Scientists have identified a molecular switch that controls the immune machinery responsible for chronic inflammation in the body. The finding could lead to new ways to halt or even reverse many age-related conditions, from from Alzheimers and Parkinsons to diabetes and cancer.
In medicine, we now understand how chronic inflammation damages healthy tissue and sets us up for deeper diseases. Many diseases, such as...
Every action contributes to health or promotes disease. Actions that promote disease create chronic inflammation, find out what choices youre making…
Reducing inflammation may lengthen our lives, reduce discomfort and spare the immune system to be more active in ways that protect us from more important issues. (717) 558-8500
Inflammation is a mechanism used by the body to respond to harmful stimuli. But when that response is excessive, the body suffers. Here, in 10 points, are the essential facts.
When I was first dx I was told that MS was an inflammatory disease of the CNS. Being naive I thought that new drugs which dampen the inflammation would solve the problem. But MS is never simple. The following research ...
Inflammation is at the root of many diseases. Knowing what it is, how it develops, and how to fix it can save your life and your lifestyle.
Contrary to what you might believe, it is often possible to reduce inflammation without having to take any drugs, many of which can cause very nasty side effects.
Medical experts discuss the potential danger of inflammation in the body, the types of diseases that can cause it, and how to identify it.
Dr. Appleton gives us a full explanation of the causes of inflammation from a functional approach and its treatment from a drugless perspective.
The latest medical buzzword is inflammation.It sells lots of drugs. But if we took charge of our wellness naturally we wouldnt have to participate in that medical carousel.
Inflammation treatment in Ardmore, PA. Inflammation information regarding causes, stages and what to do is available through your local doctor.
Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.
Squamous cell carcinoma (SCC) is one of the most common human cancers worldwide. In SCC, tumour development is accompanied by an immune response that leads to massive tumour infiltration by inflammatory cells, and consequently, local and systemic production of cytokines, chemokines and other mediators. Studies in both humans and animal models indicate that imbalances in these inflammatory mediators are associated with cancer development. We used a multistage model of SCC to examine the involvement of elastase (ELA), myeloperoxidase (MPO), nitric oxide (NO), cytokines (IL-6, IL-10, IL-13, IL-17, TGF-β and TNF-α), and neutrophils and macrophages in tumour development. ELA and MPO activity and NO, IL-10, IL −17, TNF-α and TGF-β levels were increased in the precancerous microenvironment. ELA and MPO activity and NO, IL-10, IL −17, TNF-α and TGF-β levels were increased in the precancerous microenvironment. Significantly higher levels of IL-6 and lower levels of IL-10 were detected at 4 weeks
The development of pressure receptors takes place during the gestation period with the rapidly adapting pressure receptors developing first then followed by the slow adapting pressure receptors (Kinkelin, Stucky, L & Koltzenburg, 1999). Although these pressure receptors are present throughout the fetal life to adulthood, their depolarization responses to chemical irritants, mechanical injury and inflammatory mediators are been found to be similar in both the fetus and adults. Pressure-sensitive receptors of different types found in the skin where they detect changes in pressures. They respond to physical contact such as brushing against a wall, mosquito landing site or any form of touch on the skin. Bunched receptors known as Merkels discs have been found to specialize in conveying information about continuous pressure exerted on the surface of the skin (Ragert, Nierhaus, Cohen & Villringer, 2008). Pacinian corpuscles respond to quick changes in touch or pressure by firing off rapid bursts of ...
Inflammation can be categorized as two types, chronic and acute. When the body is exposed to harmful stimuli, such as an injury, bacteria or a foreign body, the immune system is triggered resulting in inflammation. This kind of immune response typically lasts for a short period of time and is known as acute inflammation. It is part of the bodys immune response and is a healthy reaction. Inflammation becomes a health problem when it transforms into a long-term, ongoing condition known as chronic inflammation. 2. Chronic Inflammation. Chronic inflammation can exist for a long time in a persons body without any noticeable symptoms. The process can be the result of three possible causes. Some types of chronic inflammation begin as a bout of acute inflammation after which the immune response does not shut off. Another cause of chronic inflammation is when the immune system launches an attack on healthy tissue by mistaking it for a pathogen. Lastly, chronic inflammation can result from the ...
p38 mitogen-activated protein kinase (MAPK) stabilises pro-inflammatory mediator mRNAs by inhibiting AU-rich element (ARE)-mediated decay. We show that in bone-marrow derived murine macrophages tristetraprolin (TTP) is necessary for the p38 MAPK-sensitive decay of several pro-inflammatory mRNAs, including cyclooxygenase-2 and the novel targets interleukin (IL)-6, and IL-1alpha. TTP(-/-) macrophages also strongly overexpress IL-10, an anti-inflammatory cytokine that constrains the production of the IL-6 despite its disregulation at the post-transcriptional level. TTP directly controls IL-10 mRNA stability, which is increased and insensitive to inhibition of p38 MAPK in TTP(-/-) macrophages. Furthermore, TTP enhances deadenylation of an IL-10 3-untranslated region RNA in vitro.
p38 mitogen-activated protein kinase (MAPK) stabilises pro-inflammatory mediator mRNAs by inhibiting AU-rich element (ARE)-mediated decay. We show that in bone-marrow derived murine macrophages tristetraprolin (TTP) is necessary for the p38 MAPK-sensitive decay of several pro-inflammatory mRNAs, including cyclooxygenase-2 and the novel targets interleukin (IL)-6, and IL-1alpha. TTP(-/-) macrophages also strongly overexpress IL-10, an anti-inflammatory cytokine that constrains the production of the IL-6 despite its disregulation at the post-transcriptional level. TTP directly controls IL-10 mRNA stability, which is increased and insensitive to inhibition of p38 MAPK in TTP(-/-) macrophages. Furthermore, TTP enhances deadenylation of an IL-10 3-untranslated region RNA in vitro.
Reading Time: 3 minutes. By: Sheila Olson - Confluence Daily is your daily news source for women in the know.. Inflammation can be beneficial to the body by signaling to your immune system that your body needs to recover from infection or injury. Sometimes, however, things can go awry, and your body can experience inflammation where it is not needed. Systemic inflammation can be debilitating and cause other problems that affect your entire body. If you struggle with systemic inflammation, all hope is not lost. There are some steps you can take to alleviate your pain.. What Is Inflammation?. Inflammation is your bodys natural way to heal itself and fight off toxins, infections, and injuries. When the cells in your body are damaged, a chemical response is triggered by your immune system, which includes releasing antibodies and proteins. Coupled with increased blood flow to the harmed area of your body, you will see acute inflammation. Inflammation should naturally decrease and go away entirely in ...
The inflammatory process.. Image: BloodJournal. Acute inflammation and chronic inflammation are different. Acute inflammation starts the minute we drop a hammer on our toe or cut a finger, or even come into contact with a virus. Its a good, natural thing.. Chronic inflammation can last for months or even years - meaning that our cells are constantly under attack. We age faster, we get sick more easily, and we can start to deteriorate because the body is fighting us instead of a real disease or injury.. The amazing reality is that we can stop chronic inflammation and allow the body to go about healing us from just about everything - from the cells to entire sets of muscle, neural tissue, and joints, by halting chronic inflammation. Lets start with herbal remedies.. You can heal inflammation with the following powerful, anti-inflammatory herbs and spices:. ...
Tohoku University scientists have found that human editing enzymes are likely behind a type of mutation in the COVID-19 virus that stimulates the release of pro-inflammatory molecules called cytokines by immune cells in the body.
During inflammation, lutein is thought to scavenge ROS generated during inflammatory process and to interfere in intracellular pathways leading to the expression of various pro-inflammatory molecules. Moreover, since the eye is constantly exposed to light (being susceptible to light-induced damage), a great deal of interest focusing on the neuroprotective role of lutein has been generated ...
I find myself talking a lot about inflammation, purchase as a result of diet and exercise. Its usually questions I receive from non-CrossFitters like: what is inflammation, and why is it bad? Does it matter?. Inflammation is actually a good, essential part of life; the response our body gets from exercise, a bump, a cut are forms of acute inflammation. What were trying to halt is chronic inflammation. Im not crazy about my answers, so Im going to do some research on inflammation. Heres some of my early reading.. What is Inflammation. How to Tell If Youre Inflamed. The Relationship Between Exercise and Inflammation.. ...
Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System in Cns Neurol Disord Drug Targetscns Neurol Disord Drug Targets ...
Chronic Inflammation is more common than you think. Chronic Inflammation can cause stroke, heart attack and even cancer. It starts as a slow burn inside of your body and acts as an emergency vehicle responding to stressors, lack of sleep, infections, injuries, allergens, a poor diet, or toxins.. The tender throbbing hot spots which may feel uncomfortable are actually part of your bodys natural response. It means your immune system is sending internal signals to launch white blood cells and protein to destroy infection and heal injuries.. But if the inflammation lingers after the job is done, or your immune system becomes confused and misfires by accident, what was once your best friend can quickly become your worst enemy.. When inflammation becomes chronic, your bodys natural defense system takes a turn for the worse by starting a sneak attack on your joints, tissue and blood vessels wreaking havoc on all those areas which were once pain free. Thats when the slow burning throb becomes a five ...
The Inflammation QuizConcerned about your inflammation levels?Take our Inflammation Quiz at the link below.Learn what factors are attributed to high inflammation, and what you can do about it.,, Continue to the Inflammation QuizAbout: We developed the Inflammation Quiz to help you assess your lifestyle behaviors and learn more about how to implement an anti-inflammatory diet […]. Continue reading ...
The problem with all of these things is that they create chronic inflammation, which is really the problem that we are all facing. With less chronic inflammation we will obviously have many fewer problems.. Acute inflammation, which is something that comes up when we go to the gym and workout, is good. This is the kind of inflammation that brings nutrients and other essential elements to a single place so that we can more adequately feed our muscles, joints, and prepare for the recovery that we need.. This is one of the reasons why some scientists believe eating vitamin C or other antioxidant and anti-inflammation supplements is actually not useful after a workout and can hurt your chances of recovery.. ...
What we put into our body doesnt just reflect how we look on the outside, but how we feel on the inside. And for many patients who come to us seeking relief care initially, they dont fully understand how poor nutrition can lead to body aches and inflammation.. So, what exactly does it mean to suffer from internal inflammation? When a substance that your body doesnt want is introduced, your immune system begins to attack it, causing inflammation that can manifest itself in a number of ways including swollen and painful joints, decreased range of motion, stress and anxiety and fatigue among others. If were constantly putting food into our bodies that it doesnt want, inflammation can become a gateway to chronic disease.. But before we get to foods that can help your body stay healthy and away from inflammation, lets take a look at foods that are known to promote it. Typically, these are foods we wouldnt consider healthy like:. ...
Health, ...COLUMBUS Ohio A new study shows how inflammation can help cause canc...This study by researchers at the Ohio State University Comprehensive C...This in turn causes a drop in levels of proteins involved in DNA rep... Our study shows that miR-155 is upregulated by inflammatory stimuli a...,Study,shows,how,inflammation,can,lead,to,cancer,,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
For thousands of years inflammation has been documented as a chief indicator of illness.Inflammation is the bodys immune system response to protecting the body from injury and infection. It signals the body into defense mood by increasing its white blood cell count to stop infection from spreading. Scientists and doctors found inflammation is positively correlated to chronic illnesses, like autoimmune diseases. It is important to understand how inflammation works and how nutrition can be integr
We are an emerging regenerative medicine company in London discovering and developing drugs targeting chronic serious intestinal inflammation at its source by correcting imbalances in cell production and function
By Jon Trister MD and Renata Trister DO. Infectious and metabolic toxemias are two major causes of chronic systemic inflammation. Acute inflammation is a rapid onset process, with more conspicuous symptoms and a short duration. Chronic inflammation, however, is more insidious. It is the result of a perpetual onslaught from a variety of toxins and pathogens. It is a long lasting process that is often silent with indistinct symptoms.. ...
Health & Wellness column: - Recent studies are pointing to chronic inflammation as being a major risk factor for heart disease. Because inflammation can be painless and frequently goes undetected, its relationship to disease has been overlooked. If you have several diseases caused by inflammation, you may have a low-level chronic inflammatory process that could eventually lead to heart disease.
Inflammation is good for the body. But sometimes, it goes out of control and begins to behave badly. Scientists have linked inflammation to heart diseases, and cancers, just to mention a few. You can get rid of inflammation by only consuming foods that are naturally endowed with the capacity to fight inflammation or discourage it…
Most of us know that inflammation is bad. But most of dont know exactly what inflammation is. Nor do we know how and why its bad. In this post, we will answer the questions what is inflammation and how does inflammation affect health.
The word inflammation is a widely misunderstood term considered to be something that causes harm to our body. The truth is, inflammation is an essential pathway of your immune system to protect your body from something as simple as a small cut to fighting a severe infection. The process of inflammation includes increased blood flow at the site of injury/infection, dilation of capillaries, white blood cell infiltration, and production of chemical mediators to manage the condition. ...
The Call mediator is used to send messages out of the Micro Integrator to an endpoint. You can invoke services either in blocking or non-blocking manner.. When you invoke a service in non-blocking mode, the underlying worker thread returns without waiting for the response. In blocking mode, the underlying worker thread gets blocked and waits for the response after sending the request to the endpoint. Call mediator in blocking mode is very much similar to the Callout mediator.. In both blocking and non-blocking modes, Call mediator behaves in a synchronous manner. Hence, mediation pauses after the service invocation, and resumes from the next mediator in the sequence when the response is received. Call mediator allows you to create your configuration independent from the underlying architecture.. Non-blocking mode of the Call mediator leverages the non-blocking transports for better performance. Therefore, it is recommended to use it in non-blocking mode as much as possible. However, there are ...
Acute inflammation is actually beneficial. But chronic inflammation is a killer. Inflammation and the different forms are important to understand.
Inflammation is the bodys healthy immune response to infections, injury or illness. Once the body finishes healing itself then the inflammation should stop Yet sometimes it doesnt. When inflammation flares up and burns out of control, this is when trouble occurs This could possibly take a toll on the rest of the body
What is chronic inflammation? Our infographic explains the causes, known treatments and warning signs of Chronic Inflammation - the Silent Killer.
Recent research suggest that chronic inflammation could be part of the PCOS picture. Find out what you can do to reduce your risk of chronic inflammation.
What is inflammation? There are two phases of the inflammatory process. Chronic low-level inflammation can ultimately lead to loss of function and cellular aging.
Newswise - Although normal inflammation plays an important role in helping to fight off infections, there is mounting evidence that chronic inflammation is linked to increased risk of tumor...
Study Flashcards On Path (4/4) MEDIATORS OF INFLAMMATION at Quickly memorize the terms, phrases and much more. makes it easy to get the grade you want!
Low-level inflammation causes millions to die every year. This type of inflammation can easily be identified with a simple blood test. Usually, it can easily be treated with a combination of all herbs and nutrients. In years to come it
Inflammation is the bodys natural defense against injury or disease. Chronic inflammation, on the other hand, is believed to be a major contributor to disease.(...)
What causes inflammation, the dangers of chronic inflammation and three anti-inflammation principles for less pain and a longer life.
Study Flashcards On Path (4/5) Acute/Chronic Inflammation at Quickly memorize the terms, phrases and much more. makes it easy to get the grade you want!
PCOS and inflammation are linked very closely. Learn more about the signs of inflammation, and tips to lower it naturally to reduce PCOS symptoms.
Looking for a solution to ease your inflammation? Shop from our selection of anti-inflammatory supplements, designed to help treat and prevent inflammation.
OA Inflammation is a multidisciplinary open access peer reviewed journal that publishes basic and clinical research concerning all aspects of inflammation and inflammatory disease.
Researchers demonstrated how inflammation can spread through the brain in a study in mice, published in the Journal of Neuroinflammation.
Are you worried your English writing doesnt seem professional?Get fluency suggestions for proper grammar, clear phrasing, natural word choice, and more. Try now!Acute inflammation is how your body fights infections and helps speed up the healing process, says Dr. Shmerling. In this way, inflammation is good because it protects the body. This process works the…. ...
XenoLight RediJect Chemiluminescent Inflammation probe (Standard Kit) for monitoring Inflammation to study myeloperoxidase (MPO) activity.
For some people, there is a violent storm going on within their bodies and they dont even know it: the storm of chronic, low-grade inflammation. Heres how to tame it.
By Justin Cowart We all know that, depending on the severity and level of inflammation, it can take a huge toll on your quality of life. Inflammation(...)
Inflammation is the root of many health problems. Add these 9 natural inflammation reducers to your diet and start feeling better, fast.
CBD for Inflammation CBD is extremely effective in managing inflammation. CBD actually stops the inflammatory cycle by decreasing the production and release of
Inflammation is one of the leading drivers of many common diseases. Here are 6 supplements that can reduce inflammation, backed by science.
Inflammation is one of the buzziest wellness words-and one of the misunderstood. Here, doctors dispel myths and share important inflammation facts.
Down to the cell level. Its where me must strive to get to if we are going to eradicate chronic disease for good. Its not good enough anymore to just do
Moreover, an increasing number of studies have investigated the role of different mediators of inflammation in the early ... In this review, we have summarized the main markers of inflammation that could be useful in diagnosis and shed some light in ... Its pathogenesis is not fully elucidated, but a pivotal role has been attributed to inflammation, strong evidence supporting ... Mediators of Inflammation - A Potential Source of Biomarkers in Oral Squamous Cell Carcinoma. Mircea Tampa. ,1,2Madalina Irina ...
The higher level of systemic inflammation and concomitant increased AF risk in Whites is not explained by racial differences in ... Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation: Results from the Health, Aging, and Body ... Both inflammation and obesity are risk factors for AF, and adipose tissue is a known contributor to systemic inflammation. ... The higher level of systemic inflammation and concomitant increased AF risk in Whites is not explained by racial differences in ...
Gram, M., Sveinsdottir, S., Cinthio, M. et al. Extracellular hemoglobin - mediator of inflammation and cell death in the ... Extracellular hemoglobin - mediator of inflammation and cell death in the choroid plexus following preterm intraventricular ... Extracellular hemoglobin - mediator of inflammation and cell death in the choroid plexus following preterm intraventricular ... Fang H, Wang PF, Zhou Y, Wang YC, Yang QW: Toll-like receptor 4 signaling in intracerebral hemorrhage-induced inflammation and ...
... Academic Article ... We hypothesized that IL-1R-associated kinase 1 (IRAK1), a key signaling mediator in the TLR/IL-1 pathway, plays a critical role ... induction of p-IRAK1 and downstream proinflammatory signaling mediators were seen in the FM. In a C57BL/6J wild-type PTB mouse ... and mouse demonstrates a critical role IRAK1 in IUI and inflammation-associated PTB and suggest it as potential therapeutic ...
Prostaglandins are mediators of inflammation. Because meloxicam is an inhibitor of prostaglandin synthesis, its mode of action ... 5.13 Masking of Inflammation and Fever. The pharmacological activity of meloxicam in reducing inflammation, and possibly fever ... 5.13 Masking of Inflammation and Fever 5.14 Laboratory Monitoring 6 ADVERSE REACTIONS 6.1 Clinical Trials Experience 6.2 ... NSAIDs are used to treat pain and redness, swelling, and heat (inflammation) from medical conditions such as different types of ...
Mediators of inflammation: complement. In: McPherson RA, Pincus MR, eds. Henrys Clinical Diagnosis and Management by ... When the complement system is turned on during inflammation, levels of complement proteins may go down. Complement activity may ...
Mediators Inflamm Ano de publicação: 2023 Tipo de documento: Artigo ... Alleviates Myocardial Ischemia-Reperfusion Injury by Protecting Endothelial Cells from Apoptosis and Inflammation. ... Mediators Inflamm Ano de publicação: 2023 Tipo de documento: Artigo ...
Dive into the research topics of Leukotrienes as mediator of allergic inflammation. Together they form a unique fingerprint. ... keywords = "Allergic inflammation, Leukotriene antagonists, Leukotrienes, Mast cells",. author = "Ollert, {M. W.} and J. Ring", ... are members of the eicosanoid family of lipid molecules that are among the most potent mediators of allergic inflammation in ... are members of the eicosanoid family of lipid molecules that are among the most potent mediators of allergic inflammation in ...
"Mediators of Inflammation. 2015: 1-7. doi:10.1155/2015/520871. PMC 4345265. PMID 25784781.. ... "Prostaglandins & Other Lipid Mediators. 108: 1-8. doi:10.1016/j.prostaglandins.2013.11.001. PMC 4004677. PMID 24315875.. ... Inflammation[edit]. HxA3 and HxB3 possess pro-inflammatory actions in, for example, stimulating human neutrophil chemotaxis and ... Murphy, R. C.; Zarini, S (2002). "Glutathione adducts of oxyeicosanoids". Prostaglandins & Other Lipid Mediators. 68-69: 471-82 ...
Role of adipogenic mediators in inflammation. Once inside the cytoplasm, the selective fatty acids are carried to different ... It appears that co-culturing pre-adipocytes with macrophages induces a shift from a pro-inflammation to an anti-inflammation ... Systemic low-grade inflammation is related to both circulating and adipose tissue TNFalpha, leptin and IL-6 levels in obese ... However, in the presence of the stress hormone cortisol, it appeared that there was a decrease in pro-inflammation and an ...
Key player in cell death moonlights as a mediator of inflammation Key player in cell death moonlights as a mediator of ...
Mediators of Inflammation. State. NE. Performing Organization. University of Nebraska Medical Center - Omaha ...
Additional mediators activate other pathways of inflammation: the neutral proteases, tryptase and chymase; proteoglycans such ... Additional mediators include newly generated lipid-derived mediators such as prostaglandin D2, leukotriene B4, and platelet- ... These mediators can activate the kallikrein-kinin contact system, the complement cascade, and coagulation pathways. The ... Certain agents are thought to cause direct nonimmunologic release of mediators from mast cells, a process not mediated by IgE. ...
Categories: Inflammation Mediators Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, ...
May depress formation, release, and activity of endogenous chemical mediators of inflammation. ... Decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. ... May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. ...
Mediators of Inflammation, Vol. 2018, Issue. , p. 1. *CrossRef. *Google Scholar. Kabadayi Sahin, Esra Caykoylu, Ali Senat, ...
Mediators of Inflammation 2018, 2018, 3972104. * Bodewes ILA, Al-Ali S, vanHelden-Seeuwsen CG, Maria NI, Tarn JR, Lendrem DW, ... Inflammation and Immunology Theme. Faculty of Medical Sciences. Newcastle University Framlington Place. Newcastle-upon-Tyne NE1 ...
Claudin-2 as a mediator of leaky gut barrier during intestinal inflammation. Tissue Barriers. 2015;3(1-2):e977176. ... de Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients. 2013;5 ... de Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients. 2013;5 ... Vitamin D deficiency promotes epithelial barrier dysfunction and intestinal inflammation. J Infect Dis. 2014;210(8):1296-1305. ...
Mediators inflammation (2020) 2020:9706140. doi: 10.1155/2020/9706140. CrossRef Full Text , Google Scholar ... There is limited evidence for the L-tryptophan role in inflammation, but it has been linked to several age-related diseases (36 ... Collier ME, Zhang S, Scrutton NS, Giorgini F. Inflammation Control and Improvement of Cognitive Function in COVID-19 Infections ... However, downregulation of L-tryptophan could provoke chronic inflammation or inflammaging, which is a significant risk factor ...
Prostaglandins are mediators of inflammation. Because naproxen is an inhibitor of prostaglandin synthesis, its mode of action ... Masking of Inflammation and Fever. The pharmacological activity of naproxen in reducing inflammation, and possibly fever, may ... NSAIDs are used to treat pain and redness, swelling, and heat (inflammation) from medical conditions such as different types of ... Gastrointestinal: inflammation, bleeding (sometimes fatal, particularly in the elderly), ulceration, perforation and ...
Mediators of Inflammation.. *Paramel, G. , Folkersen, L. , Strawbridge, R. J. , Elmabsout, A. , Särndahl, E. , Lundman, P. , ... Genetiska variationer gener associerade med inflammation och predisposition för förändrade biomarkörprofiler * Inflammation and ... Inflammation i blodkärlens väggar leder till att kärlväggarna stelnar och blir tjocka, vilket i in tur orsakar ateroskleros, ... Betydelsen av CARD8 för inflammation i vaskulära celler * Betydelsen av NLRP3 inflammasome och interleukin-1 (IL-1) vid ...
Anti-Inflammatory Agents, Antirheumatic Agents, and Inflammation Mediators. Anti-Inflammatory Agents. Antibiotics, Glycopeptide ...
Prostaglandins are mediators of inflammation. Because diclofenac is an inhibitor of prostaglandin synthesis, its mode of action ... 5.13 Masking of Inflammation and Fever. The pharmacological activity of Diclofenac Potassium in reducing inflammation, and ... 5.13 Masking of Inflammation and Fever 5.14 Laboratory Monitoring 6 ADVERSE REACTIONS 6.1 Clinical Trials Experience 7 DRUG ... NSAIDs are used to treat pain and redness, swelling, and heat (inflammation) from medical conditions such as different types of ...
Antiarthritic effect of bee venom: Inhibition of inflammation mediator generation by suppression of NF-κB through interaction ... Antiarthritic effect of bee venom: Inhibition of inflammation mediator generation by suppression of NF-κB through interaction ...
... which is a potent NF-kappaB activator and as such can intensify inflammation and renal injury. This supposition is supported by ... which is a potent NF-kappaB activator and as such can intensify inflammation and renal injury. Oxidative stress plays an ... Excreted urinary mediators in an animal model of experimental immune nephritis with potential pathogenic significance.. *Tianfu ... OXR1-MSCs transplantation may exert a certain protective effect on nephritis by suppressing inflammation and oxidative stress. ...
Despite a lack of difference in circulating markers of inflammation (hsCRP, IL-6, and bioactive lipid mediators), vascular ... Cellular and Circulating Markers of Oxidative Stress, Inflammation, and Bioactive Lipid Mediators. Cellular Markers.. Vascular ... Circulating markers of oxidative stress, inflammation, and bioactive lipid mediators were previously shown to be altered in ... Circulating Markers of Oxidative Stress, Inflammation, and Bioactive Lipid Mediators.. Serum high-sensitivity C-reactive ...

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