Pathobiochemical mechanisms during the acute phase response.
The acute phase response is characterised by the following sequence of principle phenomena: (1) an early local inflammatory reaction, (2) formation of inflammatory humoral factors inducing a systemic reaction, (3) stimulation of glycoprotein synthesis predominantly in the hepatocytes, and (4) an increase in the plasma concentration of acute phase proteins, when the rate of biosynthesis exceeds the degradation rate. Inflammatory mediators (lysosomal enzymes, oxygen derived radicals, prostaglandins) are mainly released during phagocytosis by granulocytes and macrophages. The signal reaching the hepatocytes is not yet clearly identified. A leukocyte endogenous mediator (LEM) released by macrophages is described. There is evidence that prostaglandins and probably proteinase alpha 2-macroglobulin complexes are also involved. The hepatic acute phase protein synthesis is modulated by hormones (insulin, cortisol, somatotropin). The biochemical events in the hepatocyte include an increase in protein synthesis and the regulatory control of the glycosylation of polypeptide precursors. The secreted glycoproteins serve variously as inhibitors or mediators of the inflammatory processes.
D000209:Acute-Phase Proteins; D000818:Animals; D001798:Blood Proteins / Q000096:biosynthesis; D001809:Blood Viscosity; D006023:Glycoproteins / Q000096:biosynthesis; D006098:Granulocytes / Q000502:physiology; D006728:Hormones / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D010196:Pancreatic Elastase / Q000037:antagonists & inhibitors; D051381:Rats
D000209:Acute-Phase Proteins; D001798:Blood Proteins; D006023:Glycoproteins; D006728:Hormones; D010196:Pancreatic Elastase