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CHEMICAL MEDIATORS OF INFLAMMATION 2 GROUPS 1.MEDIATORS RELEASED BY CELLS 2.MEDIATORS DERIVED FROM PLASMA. CHEMICAL MEDIATORS OF INFLAMMATION CELL DERIVED MEDIATORS 1.VASOACTIVE AMINES-HISTAMINE AND SEROTONIN HISTAMINE PRESENT IN GRANULES OF MAST CELLS, BASOPHILS AND PLATELETS. VARIOUS AGENTS WHICH RELEASE HISTAMINE FROM THESE CELLS ARE HISTAMINE A.STIMULI LIKE HEAT , COLD , IRRADIATION,TRAUMA,IRRITANT CHEMICALS,IMMUNOLOGICAL REACTIONS. HISTAMINE B.ANAPHYLATOXINS-COMPLIMENT FRAGMENTS-C3a ,C5a C.HISTAMINE RELEASING FACTORS FROM NEUTROPHILS,MONOCYTES, PLATELETS HISTAMINE D. NEUROPEPTIDES-SUBSTANCE P E. INTERLEUKINS HISTAMINE ACTION OF HISTAMINEVASODILATATION, INCREASED VASCULAR PERMEABILITY, ITCHING AND PAIN VASOACTIVE AMINES SEROTONIN(5HT) VASOACTIVE AMINES SEROTONIN(5HT)PRESENT IN CHROMAFFIN CELLS OF GIT,SPLEEN, NERVOUS TISSUE, MAST CELLS AND PLATELETS VASOACTIVE AMINES SEROTONIN(5HT) ACTION IS SIMILAR TO HISTAMINE BUT IT IS LESS POTENT MEDIATOR OF INCREASED VASCULAR PERMEABILITY AND VASODILATATION 2.ARACHIDONIC ACID METABOLITES(EICOSANOIDS) 2 PATHWAYS OF ACTIVASION1.CYCLOOXYGENASE PATHWAY AND 2.LIPO-OXYGENASE PATHWAY EICOSANOIDS METABOLITES OF CYCLO-OXYGENASE(A FATTY ACID ENZYME) PATHWAY PROSTAGLANDINS, THROMBOXANE A2 & PROSTACYCLIN. 1.PROSTAGLNDINSPGD2,PGE2, PGF2α EICOSANOIDS METABOLITES OF CYCLO-OXYGENASE(A FATTY ACID ENZYME) PATHWAY PGD2 AND PGE2-CAUSE INCREASED VENULAR PERMEABILITY, VASODILATATION, BRONCHODILATATION, INHIBIT INFLAMMATORY CELL FUNCTION ARACHIDONIC ACID METABOLITES METABOLITES OF LIPO-OXYGENASE PATHWAY LIPO-OXYGENASE ENZYME ACT ON ACTIVATED ARACHIDONIC ACID TO FORM HYDROPEROXY COMPOUND, 5-HPETE WHICH ON FURTHER PEROXYDATION FORMS 2 METABOLITES ARACHIDONIC ACID METABOLITES METABOLITES OF LIPO-OXYGENASE PATHWAY A.5HETE - CHEMOTACTIC AGENT FOR NEUTROPHILS B.LEUKOTRIENS OR SLOW REACTING SUBSTANCES OF ANAPHYLAXIS- METABOLITES OF LIPO-OXYGENASE PATHWAY LTA4 - UNSTABLE LTB4 - CHEMOTACTIC FOR PHAGOCYTES METABOLITES OF LIPO-OXYGENASE PATHWAY LTC4 , LTD4 , LTE4VASOCONSTRICTION, BRONCHOCONSTRICTION, INCREASED VASCULAR PERMEABILITY 3.LYSOSOMAL COMPONENTS INFLAMMATORY CELLS -NEUTROPHILS AND MONOCYTES CONTAIN LYSOSOMAL GRANULES WHICH RELEASE A VARIETY OF MEDIATORS OF INFLAMMATION 3.LYSOSOMAL COMPONENTS GRANULES OF NEUTROPHILS A.SPECIFIC OR SECONDARY-CONTAIN LACTOFERRIN,LYSOZYME, ALKALINE PHOSPHATASE, COLLAGENASE 3.LYSOSOMAL COMPONENTS B.LARGE PRIMARY GRANULES AZUROPHIL GRANULES HAVE MYELOPEROXIDASE, ACID HYDROLASES WHICH DESTROY PHAGOLYSOSOMAL CONTENT 3.LYSOSOMAL COMPONENTS NEUTRAL PROTEASES SUCH AS ELASTASE,COLLAGENASE AND PROTEINASE WHICH ATTACK EXTRACELLULAR CONSTITUENTS SUCH AS BASEMENT MEMBRANE,COLLAGEN, ELASTIN,CARTILAGE 3.LYSOSOMAL COMPONENTS GRANULES OF MONOCYTES AND TISSUE MACROPHAGES RELEASE ACID PROTEASES, COLLAGENASES, 3.LYSOSOMAL COMPONENTS ELASTASE AND PLASMINOGEN ACTIVATOR. THEY ARE MORE ACTIVE IN CHRONIC INFLAMMATION 4.PLATELET ACTIVATING FACTOR(PAF) RELEASED FROM IgE SENSITISED BASOPHILS OR MAST CELLS,OTHER LEUKOCYTES,ENDOTHELIAL CELLS,AND PLATELETS.CAUSE PLATELET AGGREGATION AND RELEASE REACTION, 4.PLATELET ACTIVATING FACTOR(PAF) INCREASED VASCULAR PERMEABILITY, VASOCONSTRICTION, VASODILATATION IN LOW CONCENTRATION, BRONCHOCONSTRICTION, 4.PLATELET ACTIVATING FACTOR(PAF) ADHESION OF LEUKOCYTES TO ENDOTHELIUM, CHEMOTAXIS 5.CYTOKINES POLYPEPTIDES PRODUCED BY ACTIVATED LYMPHOCYTES(LYMPHOKINES) AND ACTIVATED MONOCYTES(MONOKINES). HAVE AUTOCRINE OR PARACRINE ACTION 5.CYTOKINES(CHEMOKINES) IL-1 AND TNF α FROM ACTIVATED MACROPHAGES, TNF-β AND IF GAMA PRODUCED BY ACTIVATED T CELLS CHEMOKINES INCLUDEIL8 AND PF4 ACTION OF CYTOKINES l. IL-1,TNFα,TNFβ – CAUSE LEUKOCYTE ADHESION, THROMBOGENICITY, FIBROBLAST PROLIFERATION, ACUTE PHASE REACTIONS ACTION OF CYTOKINES ll. IF GAMA - ACTIVATION OF MACROPHAGES,NEUTROPHILS, SYNTHESIS OF NITRIC OXIDE ACTION OF CYTOKINES iii. CHEMOKINES CHEMOKINESARE A FAMILY OF CHEMOATTRACTANTS FOR INFLAMMATORY CELLS 1. IL-8 CHEMOTACTIC FOR NEUTROPHILS ACTION OF CYTOKINES 2. PLATELET FACTOR 4 - CHEMOTACTIC FOR NEUTROPHILS,MONOCYTES AND EOSINOPHILS 3.MCP-1- FOR MONOCYTES 4.EOTAXIN- CHEMOTACTIC FOR EOSINOPHILS 6.NITRIC OXIDE AND OXYGEN METABOLITES NO - PRODUCED BY ENDOTHELIAL CELLS AND ACTIVATED MACROPHAGES ACTIONS VASODILATATION, ANTIPLATELET ACTIVATING AGENT MICROBICIDAL ACTION 7.OXYGEN DERIVED METABOLITES FROM ACTIVATED NEUTROPHILS AND MACROPHAGES OXYGEN DERIVED FREE RADICALS HAVE FOLLOWING ACTION IN INFLAMMATION a. ENDOTHELIAL CELL DAMAGE- INCREASED PERMEABILITY OXYGEN METABOLITES b. ACTIVATION OF PROTEASE AND INACTIVATION OF ANTIPROTEASETISSUE MATRIX DAMAGE,DAMAGE TO OTHER CELLS FREE RADICALS ARE COUNTERACTED BY ANTIOXIDANTS ANTIOXIDANTS ARE ENDOGENOUS & EXOGENOUS SUBSTANCES WHICH INACTIVATES FREE RADICALS- ANTIOXIDANTS 1.VITAMINS E,A, C 2.SULFHYDRIL CONTAINING COMPOUNDSCYSTEIN,GLUTATHIONE 3 SERUM PROTEINS-CERULOPLASMIN & TRANSFERRIN 11 .PLASMA DERIVED MEDIATORS PLASMA PROTEASES PRODUCED BY ACTIVATION AND INTERACTION OF 4 INTERLINKED SYSTEM KININ, CLOTTING, FIBRINOLYTIC AND COMPLIMENT SYSTEM PLASMA DERIVED MEDIATORS PLASMA PROTEASES HAGEMAN FACTOR(F-XII)-ACTIVATED BY CONTACT WITH BASEMENT MEMBRANE AND BACTERIAL ENDOTOXINS IN VIVO LEADS TO PLASMA DERIVED MEDIATORS PLASMA PROTEASES ACTIVATION OF CLOTTING, FIBRINOLYTIC, AND KININ SYSTEMEND PRODUCTS OF ACTIVATION OF THESE SYSTEMS GENERATE PERMEABILITY FACTORS WHICH FURTHER ACTIVATE CLOTTING SYSTEM COAGULATION SYSTEM 1.THE KININ SYSTEM ON ACTIVATION BY FACTOR XIIa-GENERATES BRADYKININ WHICH CAUSESMOOTH MUSCLE CONTRACTION, VASODILATATION, INCREASED VASCULAR PERMEABILITY AND PAIN 2.THE FIBRINOLYTIC SYSTEM ACTIVATED BY PLASMINOGEN ACTIVATERCONVERTS PLASMINOGEN TO PLASMIN 2.THE FIBRINOLYTIC SYSTEM ACTIONS OF PLASMIN DEGRADES FIBRIN TO FIBRIN SPLIT PRODUCTS WHICH INCREASE VASCULAR PERMEABILITY,CHEMOTAXIS TO LEUKOCYTES 3.THE CLOTTING SYSTEM ACTIVATED BY XIIa- RELEASE FIBRIN AND FIBRINOPEPTIDESWHICH CAUSE INCREASED VASCULAR PERMEABILITY, CHEMOTAXIS, ANTICOAGULANT ACTIVITY 4.THE COMPLEMENT SYSTEM ACTIVATION OF COMPLEMENT PATHWAYS RELEASE ANAPHYLATOXINS-C3a,C4a,C5a - MAST CELLS TO RELEASE VASOACTIVE AMINES THE COMPLEMENT SYSTEM ACTIONS OF ANAPHYLATOXINS RELEASE OF HISTAMINES FROM MAST CELLS AND BASOPHILS - CAUSE INCREASED VASCULAR PERMEABILITYOEDEMA THE COMPLEMENT SYSTEM C3b AUGMENTS PHAGOCYTOSIS C5a-CHEMOTACTIC FOR LEUKOCYTES 2. MAC–MEMBRANE ATTACK COMPLEX CAUSES PORES IN THE CELL MEMBRANE OF MICROORGANISMS