Inflammation and immunity relation Essay
Inflammation and immunity relation
Relation between inflammation and immunity
Tissue damage elicits an inflammatory response, which comprises the rapid synthesis of acute phase molecules. The early local response shapes the resolution of inflammation. Pentraxins are evolutionary conserved soluble pattern recognition receptors, produced in the liver (e.g. C-reactive protein) or at sites of inflammation. Pentraxins behave as flexible adaptors of innate cell functions, complement activation and clearance of cell and matrix debris, regulating tissue hyperplasia and scarring and limiting the risk of autoimmunity associated to unscheduled cell death in vivo (Manfredi et al, 2008).
Difference between inflammation and immunity
Cell components that are released by necrotic cells elicit local and systemic inflammatory responses. Accordingly, the inflammatory activity of dying cells decays over time, as soon these alarm signals, which cannot be replenished, are degraded. A group of them, heterogeneous in terms of structure, intracellular function and localization, are believed to be endowed with intrinsic inflammatory action 15 M.E. Bianchi and A.A. Manfredi, High-mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity, Immunol Rev 220 (2007), pp. 35–46. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (5)and they include the nuclear protein, HMGB1, the endproduct
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What is the purpose of inflammation?
All cells of the immune system are main actors of the inflammatory process. They cross talk by means of chemical messengers including cytokines and chemokines. In an inflammatory site, hundreds of mediators are produced in and around the cells acting on local vascular endothelium, causing vessel dilatation, fluid leakage and migration of neutrophils and monocytes/macrophages from the blood into the tissue. This causes redness, heat, swelling and pain, which are the four attributes of an inflammatory reaction. Innate immune responses also include the synthesis of anti-microbial peptides that are capable of directly killing a variety of pathogens by disrupting their cytoplasmic membrane (Yeretssian et al, 2008).
Tissue injury is a critical initiator of the acute phase response. Platelets aggregate at the ends of injured vessels, converting fibrinogen to fibrin and preventing the loss of blood. Neutrophils are attracted and activated, limiting the infection by bystander microorganisms. Later on macrophages clear the injured site of all debris, including fibrin and dead parenchimal and inflammatory cells and orchestrate angiogenesis and tissue remodelling. Inflammation is dramatically important for successful tissue repair (Mori et al, 2008).
Davis, H., Halablab, M.A., Young, T.W.K., Cox, F.E.G., and J, Clark (1998) Infection and Immunity, CRC Press, P.237
Manfredi, A.A., Querini, P.R., Bottazzi, B., Garlanda, C., and A. Mantovani (2008) Pentraxin, humoral innate immunity, and tissue injury, Current opinion in Immunology, Vol.20, issue 5, pp.538-544
Mori, R., Shaw, T.J., and P. Martin (2008) Molecular mechanisms linking wound inflammation and fibrosis: knockdown of osteopontin leads to rapid repair and reduced scarring, Journal of Experimental Medicine, Vol.205, pp. 43–51
Yeretssian, G., Labbe, K., and M.Saleh. (2008) Molecular regulation of inflammation and cell death, Cytokine, Article in press, Available online 13th Aug