Increased adhesion molecule expression in serosal fibroblasts isolated from patients with inflammatory bowel disease is secondary to inflammation.

Objective To examine the expression of adhesion molecules by serosal and dermal fibroblasts in patients with inflammatory bowel disease. Summary Background Data The pathophysiologic process that leads to stricture formation in Crohn's disease (CD) is unknown. Serosal fibroblasts in these patients have an enhanced ability to contract collagen. This property may be reflected in fibroblast adhesion molecule expression, which in turn may be constitutive or secondary to the inflammatory process in patients with CD. Methods Fibroblasts were isolated from inflamed and macroscopically normal serosa of patients with CD or ulcerative colitis (UC) and from normal serosa of patients with colon cancer. Dermal fibroblasts were also isolated from the wound edge. Cell surface and whole cell expression of ICAM-1 were evaluated by flow cytometry and Western blot analysis, respectively. NFkappaB was measured by mobility shift assay in parallel experiments. Interleukin I was added to the culture medium. Results Expression of ICAM-1 and NFkappaB, increased in patients with both CD and UC, was unaltered by interleukin 1beta. The whole cell concentration of ICAM-1 was greater in patients with CD than in patients with UC. Dermal fibroblasts did not display these features. Conclusions Patients with inflammatory bowel disease display enhanced ICAM-1 expression in serosal fibroblasts but not dermal fibroblasts, indicating a secondary response to inflammation.