Mechanisms of tissue damage in inflammatory bowel disease

Crohn disease and ulcerative colitis are caused by an excessive immune-infl ammatory reaction in the intestinal wall. Analysis of the types of immune r esponse ongoing in the inflamed intestine has revealed that in Crohn diseas e there is predominantly a T helper cell type 1 response, with exaggerated production of interleukin (IL)-12 and interferon-gamma, whereas in ulcerati ve colitis the lesion seems to be more of an antibody-mediated hypersensiti vity reaction. Despite these differences, downstream inflammatory events ar e probably similar in both conditions. In both Crohn disease and ulcerative colitis there is an increased synthesis of proinflammatory cytokines, incl uding IL-1 beta, IL-6, IL-8, IL-16, and tumor necrosis factor-alpha accompa nying the influx of nonspecific inflammatory cells into the mucosa, These c ytokines contribute to the tissue damage either directly or indirectly by e nhancing the production of matrix metalloproteinases and growth factors, wh ich produce ulceration as well as mucosal repair.