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Complement Associated Diseases (view source)
Revision as of 10:39, 6 September 2007
, 10:39, 6 September 2007→BIOLOGICAL ACTIVITIES OF COMPLEMENT COMPONENTS
*** Causes cell lysis by osmotic shock.
*** Causes cell lysis by osmotic shock.
==BIOLOGICAL ACTIVITIES OF COMPLEMENT COMPONENTS==
==Biological Activities of Complement Components==
Once the complement system has been triggered it deposits a shell of protein on the bacterial cell surface. The complex is anchored to surfaces by active binding sites present on the C4b, C3b, C5b and C7 molecules. The major protein on the pathogen cell surface is iC3b. This and some of the smaller C3 breakdown products (e.g. C3d) act as targets for phagocytosis as there are very avid receptors on phagocyte membranes for these complement fragments. Complement-mediated opsonization of microorganisms is several thousand times more efficient that innate receptors. In addition the complement fragments released after complement (C2a C3a, C4a and especially C5a) are chemotactic for phagocytes. The smaller peptides (C3a and C5a) are also very efficient at inducing inflammation. Not only do they attract granulocytes to the site of complement activation but also stimulation their degranulation. Finally, the later components (C5 – C9) can kill pathogens directly by causing cell lysis. In clinical terms, this is effective against encapsulated bacterial infection like Neisseria and Meningococci.
Once the complement system has been triggered it deposits a shell of protein on the bacterial cell surface. The complex is anchored to surfaces by active binding sites present on the C4b, C3b, C5b and C7 molecules. The major protein on the pathogen cell surface is iC3b. This and some of the smaller C3 breakdown products (e.g. C3d) act as targets for phagocytosis as there are very avid receptors on phagocyte membranes for these complement fragments. Complement-mediated opsonization of microorganisms is several thousand times more efficient that innate receptors. In addition the complement fragments released after complement (C2a C3a, C4a and especially C5a) are chemotactic for phagocytes. The smaller peptides (C3a and C5a) are also very efficient at inducing inflammation. Not only do they attract granulocytes to the site of complement activation but also stimulation their degranulation. Finally, the later components (C5 – C9) can kill pathogens directly by causing cell lysis. In clinical terms, this is effective against encapsulated bacterial infection like Neisseria and Meningococci.