Mediating systems in inflammatory disease.
This article reviews the mediation systems participating or potentially participating in inflammatory disease, especially in immunologic injury of the glomerulus. Mediator systems are separated into 3 mechanisms: the first involves complement and neutrophils; the second involves systems unrelated to neutrophils and complement components from C3 to C9; and the third involves blood monocytes. Major emphasis is given to an analysis of factors that potentially participate in the second mechanism. These include humoral factors such as the coagulation system and Hageman factor systems and cellular factor such as platelets or cells resident in the glomerulus. Studies on a role of vasoactive amines are presented. The importance of separating neutrophil-dependent and -independent mechanisms in these studies is emphasized. A review of current knowledge of the biochemical mechanisms involved in the Hageman factor system is presented because of the potential role of these components in the development of inflammation.
D000818:Animals; D001485:Basement Membrane / Q000276:immunology; D003165:Complement System Proteins / Q000502:physiology; D005174:Factor XII / Q000502:physiology; D005337:Fibrin / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D005921:Glomerulonephritis / Q000276:immunology; D007105:Immune Complex Diseases / Q000150:complications; D007249:Inflammation / Q000276:immunology*; D007437:Intrinsic Factor / Q000502:physiology; D007678:Kidney Glomerulus / Q000276:immunology* / Q000293:injuries; D009393:Nephritis / Q000276:immunology; D011817:Rabbits; D051381:Rats
D005174:Factor XII; D005337:Fibrin; D005340:Fibrinogen; D003165:Complement System Proteins; D007437:Intrinsic Factor