Intestinal fibrosis in human and experimental inflammatory bowel disease

Fibrosis is a serious complication of Crohn disease for which there is no e ffective therapy, It is unclear why fibrosis, particularly fibrosis of the mucosal layer, develops in Crohn disease and not in ulcerative colitis. Smo oth muscle cells, subepithelial myofibroblasts, and fibroblasts have tradit ionally been considered mediators of fibrosis, but new information points t o a role of interstitial cells of Cajal and mast cells, Recent evidence abo ut the role of each of these cell types in fibrosis in Crohn disease or oth er inflammatory bowel diseases is described. Hypothetical models to describ e how altered function of these cells could underlie fibrosis of the mucosa or submucosal layers are presented. Fibrosis is not well characterized in any animal model of inflammatory bowel disease, The merits of several anima l models for defining the mechanisms of inflammation-induced intestinal fib rosis are reviewed.