Inflammation location, but not type, determines the increase in TGF-beta 1and IGF-1 expression and collagen deposition in IBD intestine

Background and Aims: Inflammatory bowel disease (IBD) is frequently complic ated by extracellular matrix (ECM) changes that may result in fibrosis. Tra nsforming growth factor (TGF)-beta1 and insulin-like growth factor (IGF)-1 mediate numerous ECM changes. Our aim was to determine whether TGF-beta1 an d IGF-1 are involved in intestinal ECM collagen regulation and what impact the inflammatory infiltrate has on their expression. Methods: TGF-beta1 and IGF-1 mRNA and protein were assessed in fibrosed Crohn's disease (CD), inf lamed CD, inflamed ulcerative colitis (UC), and control intestine using in situ hybridization and immunohistochemistry. Collagen types I and III were quantified by electron immunohistochemistry. Results: In CD, increased TGF- beta1 and IGF-1 mRNA expression was transmural. In UC, the increase was con fined to the lamina propria and submucosa. In both, distribution of TGF-bet a1 and IGF-1 protein matched mRNA expression and coincided with the distrib ution of the inflammatory infiltrate. An increase in the collagen type III: I ratio in both CD and UC also coincided with the inflammatory infiltrate. Conclusions: These findings suggest that TGF-beta1 and IGF-1 are involved i n intestinal ECM remodeling in IBD, and their enhanced expression depends o n the presence and location of inflammatory infiltrates rather than the typ e of IBD.