Intestinal fibrosis in human and experimental inflammatory bowel disease

Fibrosis is a serious complication of Crohn disease for which there is no effective therapy. It is unclear why fibrosis, particularly fibrosis of the mucosal layer, develops in Crohn disease and not in ulcerative colitis. Smooth muscle cells, subepithelial myofibroblasts, and fibroblasts have traditionally been considered mediators of fibrosis, but new information points to a role of interstitial cells of Cajal and mast cells. Recent evidence about the role of each of these cell types in fibrosis in Crohn disease or other inflammatory bowel diseases is described. Hypothetical models to describe 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 animal models for defining the mechanisms of inflammation-induced intestinal fibrosis are reviewed.