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Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
Chemical mediators of immunity
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Chemical mediators of immunity

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CHEMICAL MEDIATORS OF IMMUNITY

CHEMICAL MEDIATORS OF IMMUNITY

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  • Most mediators act through cell surface receptors. Exceptions are those that have a direct enzymatic effect (lysosomal enzymes) or direct toxic effect (reactive oxygen species).Stimulus response coupling leads to biological response.Mediators can stimulate target cells to release secondary mediators.Mediators are short lived. They are rapidly inactivated (helps prevent harmful effects).
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    • 1. PLASMA DERIVED MEDIATORS
    • 2.  Most mediators act through cell surface receptors. Exceptions are those that have a direct enzymatic effect (lysosomal enzymes) or direct toxic effect (reactive oxygen species).  Stimulus response coupling leads to biological response.  Mediators can stimulate target cells to release secondary mediators.  Mediators are short lived. They are rapidly inactivated (helps prevent harmful effects).
    • 3.  Series of inactive proteins circulating in the plasma that are converted to proteolytic enzymes that activate other proteins.  Plasma Proteases:  Interrelated systems that are triggered by activation of Hageman factor (Factor XII of the coagulation cascade). Activated by endotoxin, activated platelets or contact of plasma with damaged tissue (collagen, basement membrane).
    • 4.  3 interrelated systems are active within this category 1. Kinin system  Highly vasoactive 2. Complement system  Vasoactive  Chemotactic 3. Clotting system  Vasoactive  Cleaves C3
    • 5.  Factor XII of intrinsic coagulation cascade  Activated by  Negatively charged surfaces  Platelets  Proteases from inflammatory cells  Causes  Coagulation  Activation of fibrinolytic system  Produces bradykinin  Activates complement  Provides an amplification system
    • 6. Activated by Hageman factor (XIIa)  Bradykinin  Release of vasoactive nonapeptide bradykinin  Generated from the plasma  Potent vasodilator  Increased vascular permeability  Contraction of smooth muscle  Produce pain  Stimulates release of histamine  Activates the arachidonic acid cascade
    • 7.  Coagulation (clotting) system  Forms a fibrinous meshwork at an injured or inflamed site  Prevents the spread of infection  Keeps microorganisms and foreign bodies at the site of greatest inflammatory cell activity  Forms a clot that stops bleeding  Provides a framework for repair and healing  Main substance is an insoluble protein called fibrin
    • 8.  results in production of thrombin, factor Xa and formation of fibrinopeptides  thrombin cleaves fibrinogen to form fibrin and enhances leukocyte adhesion  fibrinopeptides are chemotactic and increase vascular permeability  factor Xa increases vascular permeability and leukocyte emigration
    • 9.  The blood clotting system or coagulation pathway, like the complement system, is a proteolytic cascade.  Each enzyme of the pathway is present in the plasma as a zymogen, in other words in an inactive form, which on activation undergoes proteolytic cleavage to release the active factor from the precursor molecule.  The coagulation pathway functions as a series of positive and negative feedback loops which control the activation process.  The ultimate goal of the pathway is to produce thrombin, which can then convert soluble fibrinogen into fibrin, which forms a clot.  The generation of thrombin can be divided into three phases, the intrinsic and extrinsic pathways that provide alternative routes for the generation of factor X, and the final common pathway which results in thrombin formation

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