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CHEMICAL MEDIATORS OF INFLAMMATION

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.

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CHEMICAL MEDIATORS OF INFLAMMATION

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  1. CHEMICAL MEDIATORS OF INFLAMMATION 2 GROUPS 1.MEDIATORS RELEASED BY CELLS 2.MEDIATORS DERIVED FROM PLASMA.

  2. CHEMICAL MEDIATORS OF INFLAMMATION CELL DERIVED MEDIATORS 1.VASOACTIVE AMINES-HISTAMINE AND SEROTONIN

  3. HISTAMINE PRESENT IN GRANULES OF MAST CELLS, BASOPHILS AND PLATELETS. VARIOUS AGENTS WHICH RELEASE HISTAMINE FROM THESE CELLS ARE

  4. HISTAMINE A.STIMULI LIKE HEAT , COLD , IRRADIATION,TRAUMA,IRRITANT CHEMICALS,IMMUNOLOGICAL REACTIONS.

  5. HISTAMINE B.ANAPHYLATOXINS-COMPLIMENT FRAGMENTS-C3a ,C5a C.HISTAMINE RELEASING FACTORS FROM NEUTROPHILS,MONOCYTES, PLATELETS

  6. HISTAMINE D. NEUROPEPTIDES-SUBSTANCE P E. INTERLEUKINS

  7. HISTAMINE ACTION OF HISTAMINE- VASODILATATION, INCREASED VASCULAR PERMEABILITY, ITCHING AND PAIN

  8. VASOACTIVE AMINES SEROTONIN(5HT) VASOACTIVE AMINES SEROTONIN(5HT)-PRESENT IN CHROMAFFIN CELLS OF GIT,SPLEEN, NERVOUS TISSUE, MAST CELLS AND PLATELETS

  9. VASOACTIVE AMINES SEROTONIN(5HT) ACTION IS SIMILAR TO HISTAMINE BUT IT IS LESS POTENT MEDIATOR OF INCREASED VASCULAR PERMEABILITY AND VASODILATATION

  10. 2.ARACHIDONIC ACID METABOLITES(EICOSANOIDS) 2 PATHWAYS OF ACTIVASION- 1.CYCLOOXYGENASE PATHWAY AND 2.LIPO-OXYGENASE PATHWAY

  11. EICOSANOIDSMETABOLITES OF CYCLO-OXYGENASE(A FATTY ACID ENZYME) PATHWAY PROSTAGLANDINS, THROMBOXANE A2 & PROSTACYCLIN. 1.PROSTAGLNDINS- PGD2,PGE2, PGF2α

  12. EICOSANOIDSMETABOLITES OF CYCLO-OXYGENASE(A FATTY ACID ENZYME) PATHWAY PGD2 AND PGE2-CAUSE INCREASED VENULAR PERMEABILITY, VASODILATATION, BRONCHODILATATION, INHIBIT INFLAMMATORY CELL FUNCTION

  13. ARACHIDONIC ACID METABOLITES

  14. 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

  15. ARACHIDONIC ACID METABOLITES

  16. METABOLITES OF LIPO-OXYGENASE PATHWAY A.5HETE - CHEMOTACTIC AGENT FOR NEUTROPHILS B.LEUKOTRIENS OR SLOW REACTING SUBSTANCES OF ANAPHYLAXIS-

  17. METABOLITES OF LIPO-OXYGENASE PATHWAY LTA4 - UNSTABLE LTB4 - CHEMOTACTIC FOR PHAGOCYTES

  18. METABOLITES OF LIPO-OXYGENASE PATHWAY LTC4 , LTD4 , LTE4- VASOCONSTRICTION, BRONCHOCONSTRICTION, INCREASED VASCULAR PERMEABILITY

  19. 3.LYSOSOMAL COMPONENTS INFLAMMATORY CELLS -NEUTROPHILS AND MONOCYTES CONTAIN LYSOSOMAL GRANULES WHICH RELEASE A VARIETY OF MEDIATORS OF INFLAMMATION

  20. 3.LYSOSOMAL COMPONENTS GRANULES OF NEUTROPHILS A.SPECIFIC OR SECONDARY-CONTAIN LACTOFERRIN,LYSOZYME, ALKALINE PHOSPHATASE, COLLAGENASE

  21. 3.LYSOSOMAL COMPONENTS B.LARGE PRIMARY GRANULES - AZUROPHIL GRANULES HAVE MYELOPEROXIDASE, ACID HYDROLASES WHICH DESTROY PHAGOLYSOSOMAL CONTENT

  22. 3.LYSOSOMAL COMPONENTS NEUTRAL PROTEASES SUCH AS ELASTASE,COLLAGENASE AND PROTEINASE WHICH ATTACK EXTRACELLULAR CONSTITUENTS SUCH AS BASEMENT MEMBRANE,COLLAGEN, ELASTIN,CARTILAGE

  23. 3.LYSOSOMAL COMPONENTS GRANULES OF MONOCYTES AND TISSUE MACROPHAGES RELEASE ACID PROTEASES, COLLAGENASES,

  24. 3.LYSOSOMAL COMPONENTS ELASTASE AND PLASMINOGEN ACTIVATOR. THEY ARE MORE ACTIVE IN CHRONIC INFLAMMATION

  25. 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,

  26. 4.PLATELET ACTIVATING FACTOR(PAF) INCREASED VASCULAR PERMEABILITY, VASOCONSTRICTION, VASODILATATION IN LOW CONCENTRATION, BRONCHOCONSTRICTION,

  27. 4.PLATELET ACTIVATING FACTOR(PAF) ADHESION OF LEUKOCYTES TO ENDOTHELIUM, CHEMOTAXIS

  28. 5.CYTOKINES POLYPEPTIDES PRODUCED BY ACTIVATED LYMPHOCYTES(LYMPHOKINES) AND ACTIVATED MONOCYTES(MONOKINES). HAVE AUTOCRINE OR PARACRINE ACTION

  29. 5.CYTOKINES(CHEMOKINES) IL-1 AND TNF α FROM ACTIVATED MACROPHAGES, TNF-β AND IF GAMA PRODUCED BY ACTIVATED T CELLS CHEMOKINES INCLUDE- IL8 AND PF4

  30. ACTION OF CYTOKINES l.IL-1,TNFα,TNFβ – CAUSE LEUKOCYTE ADHESION, THROMBOGENICITY, FIBROBLAST PROLIFERATION, ACUTE PHASE REACTIONS

  31. ACTION OF CYTOKINES ll. IF GAMA - ACTIVATION OF MACROPHAGES,NEUTROPHILS, SYNTHESIS OF NITRIC OXIDE

  32. ACTION OF CYTOKINESiii. CHEMOKINES CHEMOKINES- ARE A FAMILY OF CHEMOATTRACTANTS FOR INFLAMMATORY CELLS 1. IL-8 CHEMOTACTIC FOR NEUTROPHILS

  33. ACTION OF CYTOKINES 2. PLATELET FACTOR 4 - CHEMOTACTIC FOR NEUTROPHILS,MONOCYTES AND EOSINOPHILS 3.MCP-1- FOR MONOCYTES 4.EOTAXIN- CHEMOTACTIC FOR EOSINOPHILS

  34. 6.NITRIC OXIDE AND OXYGEN METABOLITES NO - PRODUCED BY ENDOTHELIAL CELLS AND ACTIVATED MACROPHAGES ACTIONS VASODILATATION, ANTIPLATELET ACTIVATING AGENT MICROBICIDAL ACTION

  35. 7.OXYGEN DERIVED METABOLITES FROM ACTIVATED NEUTROPHILS AND MACROPHAGES OXYGEN DERIVED FREE RADICALS HAVE FOLLOWING ACTION IN INFLAMMATION a. ENDOTHELIAL CELL DAMAGE- INCREASED PERMEABILITY

  36. OXYGEN METABOLITES b.ACTIVATION OF PROTEASE AND INACTIVATION OF ANTIPROTEASE- TISSUE MATRIX DAMAGE,DAMAGE TO OTHER CELLS FREE RADICALS ARE COUNTERACTED BY ANTIOXIDANTS

  37. ANTIOXIDANTS ARE ENDOGENOUS & EXOGENOUS SUBSTANCES WHICH INACTIVATES FREE RADICALS-

  38. ANTIOXIDANTS 1.VITAMINS E,A, C 2.SULFHYDRIL CONTAINING COMPOUNDS-CYSTEIN,GLUTATHIONE 3 SERUM PROTEINS-CERULOPLASMIN & TRANSFERRIN

  39. 11 .PLASMA DERIVED MEDIATORS PLASMA PROTEASES PRODUCED BY ACTIVATION AND INTERACTION OF 4 INTERLINKED SYSTEM KININ, CLOTTING, FIBRINOLYTIC AND COMPLIMENT SYSTEM

  40. PLASMA DERIVED MEDIATORSPLASMA PROTEASES HAGEMAN FACTOR(F-XII)-ACTIVATED BY CONTACT WITH BASEMENT MEMBRANE AND BACTERIAL ENDOTOXINS IN VIVO LEADS TO

  41. PLASMA DERIVED MEDIATORSPLASMA PROTEASES ACTIVATION OF CLOTTING, FIBRINOLYTIC, AND KININ SYSTEM- END PRODUCTS OF ACTIVATION OF THESE SYSTEMS GENERATE PERMEABILITY FACTORS WHICH FURTHER ACTIVATE CLOTTING SYSTEM

  42. COAGULATION SYSTEM

  43. 1.THE KININ SYSTEM ON ACTIVATION BY FACTOR XIIa-GENERATES BRADYKININ WHICH CAUSE- SMOOTH MUSCLE CONTRACTION, VASODILATATION, INCREASED VASCULAR PERMEABILITY AND PAIN

  44. 2.THE FIBRINOLYTIC SYSTEM ACTIVATED BY PLASMINOGEN ACTIVATER- CONVERTS PLASMINOGEN TO PLASMIN

  45. 2.THE FIBRINOLYTIC SYSTEM ACTIONS OF PLASMIN DEGRADES FIBRIN TO FIBRIN SPLIT PRODUCTS WHICH INCREASE VASCULAR PERMEABILITY,CHEMOTAXIS TO LEUKOCYTES

  46. 3.THE CLOTTING SYSTEM ACTIVATED BY XIIa- RELEASE FIBRIN AND FIBRINOPEPTIDES- WHICH CAUSE INCREASED VASCULAR PERMEABILITY, CHEMOTAXIS, ANTICOAGULANT ACTIVITY

  47. 4.THE COMPLEMENT SYSTEM ACTIVATION OF COMPLEMENT PATHWAYS RELEASE ANAPHYLATOXINS-C3a,C4a,C5a - MAST CELLS TO RELEASE VASOACTIVE AMINES

  48. THE COMPLEMENT SYSTEM ACTIONS OF ANAPHYLATOXINS - RELEASE OF HISTAMINES FROM MAST CELLS AND BASOPHILS - CAUSE INCREASED VASCULAR PERMEABILITY- OEDEMA

  49. THE COMPLEMENT SYSTEM C3b AUGMENTS PHAGOCYTOSIS C5a-CHEMOTACTIC FOR LEUKOCYTES 2. MAC–MEMBRANE ATTACK COMPLEX - CAUSES PORES IN THE CELL MEMBRANE OF MICROORGANISMS

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