Complement pathway activation

Activation of complement results in the generation of proinflammatory products which may ultimately lead to tissue destruction. Various studies have demonstrated the possible role of complement in tissue damage in ulcerative colitis. Monoclonal antibodies against a neoepitope exclusively expressed by activated C3b and the cytolytically active terminal complement complex have been used to identify potential complement-induced damage in tissue sections from inflamed IBD intestine. Eighty per cent (9 of 11) of patients with ulcerative colitis showed activated C3b deposited apically on the surface epithelium of involved mucosa. No deposits were seen in 31 matched noninflamed specimens or in 94% (16 of 17) of healthy controls. Strong colocalization of IgGl, activated C3b, and terminal complement complex was shown in 36% (4 of 11) of ulcerative colitis patients. Moreover, increased vascular deposition of terminal complement complexes occurred in both ulcerative colitis and Crohn's disease. Both C3 and C4 levels are elevated in jejunal perfusates of Crohn's disease patients when compared to healthy controls. Complement activation may initiate acute as well as chronic destruction of intestinal tissues and may result in the enhanced activation of granulocytes and macrophages leading to the increased release of potent chemotactic molecules by neutrophils (Figure 3).

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