Plasma derived chemical mediators of inflammation - ttylim

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Information about Plasma derived chemical mediators of inflammation - ttylim
Healthcare

Published on May 31, 2014

Author: ttylim

Source: slideshare.net

Description

describing clotting cascade, complement system, fibrinolytic system and their interrelations.

  BY : Izatty Lim (0308188)

 Able to describe the 3 systems of the plasma protein- derived mediator of inflammation.  Identify the plasma protein-derived mediator in the 3 systems and their actions.

 Definition :any messenger that acts on blood vessels, inflammatory cells or other cells to contribute to an inflammatory response. MEDIATORS

 Circulating protein of 3 interrelated system : o Complement system o Kinin system o Coagulation system

 Consist of plasma protein that play important role in host defense & inflammation.  C1 – C9  Activated by proteolysis to acquire their own proteolytic activity, thus setting up an enzymatic cascade.  Critical step : activation of 3rd component, C3, by o Classical pathway • By fixation of C1 to antigen-antibody complexes o Alternative pathway • Triggered by bacterial polysaccharides (eg. Endotoxin) & other bacterial cell wall component • Involving distinct set of plasma protein including properdin & factors B and D. o Lectin pathway • Plasma lectin bind to mannose residues on microbes & activates the early component of classical pathway

CLASSICAL PATHWAY ALTERNATIVE PATHWAY LECTIN PATHWAY Formation of C3 Convertase C 3 a C 3 b C6 – C9 Formation of C5 Convertase C 5 bC 5 a Deposit on cell/microbial surface & bind with C3 convertase (4) MAC (made up of multiple copies of final component C9) create pores  disrupt osmotic balance  cell lysis (1) VASCULAR EFFECTS: -C3a & C5a induce release of histamine -↑ vascular permeability & cause vasodilation -C5a also activates lipoxygenase pathway of AA (2) LEUKOCYTE ACTIVATION, ADHESION & CHEMOTAXIS: -C5a, C3a & C4a (lesser extent) -potent chemotatic agent for neutrophils, monocytes, eosinophil & basophil. (3) PHAGOCYTOSIS: -C3b & iC3b act as opsonins - ↑ phagocytosis

 Vascular effects (C3a & C5a)  Leukocyte activation, adhesion, chemotaxis (C5a)  Phagocytosis (C3b,iC3b)  MAC ( C9)

 Hageman factor ( Factor XII ) o A protein synthesized by the liver o Circulate in inactive form in plasma o Activated by collagen, basement membrane or activated platelets o Activated Hageman factor (factor XIIa) further actives: • Kinin system (vasoactive kinins) • Clotting system (activation of thrombin, fibrinopeptides & factor X) • Fibrinolytic system (plasmin production & inactivating thrombin) • Complement system (anaphylatoxins C3a & C5a)

(High molecular-weight kininogen)

 Bradykinin o ↑ vascular permeability o Arteriolar dilation o Branchial smooth muscle contraction o Pain  Kallikrein o Chemotatic activity o Potent activator of Hageman factor  link with clotting system HMW KININOGEN BRADYKININ KALLIKREIN

 Activated thrombin o Fibrin clot o Enhance leukocytes adhesion o Cleave C5  C5a ( link with complement system )  Fibrinopeptide o ↑ vascular permeability o Chemotatic for leukocytes  Factor Xa (intermediate in clotting cascade) o ↑ vascular permeability & leukocyte emigration Fibrinogen Activated thrombinThrombin Fibrin Clot Fibrinopeptide

 Plasmin o Multifunctional protease that cleaves fibrin o Fibrin degradation product will ↑ permeability o Cleaves C3  C3a (vasodilation & ↑ vascular permeability) o Activate Hageman factor, thus amplify the entire set of responses • Activated concurrently with activation of clotting system • Serve to limit clotting

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