A protein molecule that helps regulate body growth may play an important role in the development and progression of Crohn's disease (CD), a chronic, incurable, and frequently disabling inflammatory bowel disorder, new research shows.
Scientists led by Dr. P. Kay Lund, professor of physiology at the University of North Carolina School of Medicine have used radioactive gene probes to find significantly increased production of insulin-like growth factor (IGF-I) in inflamed and thickened intestinal tissue samples of CD patients but not in otherwise healthy bowel tissue from the same individuals. The tissue came from patients during bowel resection surgery.
"Somehow the gene for IGF-I was switched on in these cells and is not switched on in normal or non-diseased cells," Lund says. She also notes finding no evidence of increased IGF-I activity in bowel tissue from surgery patients with ulcerative colitis, the second major inflammatory bowel disorder, one that involves only the colon.
Lund says the bowel in some CD patients "tries to overgrow, something goes wrong and the structural support elements of the tissue grow excessively, and so you get a bowel that's thickened and obstructed because the wrong cells grow. This abberrant growth is termed fibrosis and is associated with deposition of lots of collagen -- a molecule associated with scarring." During this thickening, whole sections of intestinal smooth muscle cells can become encased in a dense overgrowth of fibrous collagen.
According to the UNC scientist, the new findings raise the possibility that
treatment aimed at blocking IGF-I in the bowel could prevent fibrosis
complications, such as intestinal stricture (narrowing) and obstruction. Such
complications frequently require removal of major portions of bowel. Since CD
often eventually reappears elsewhere in the bowel, surgeries for recurrent
complications can result in "short bowel syndrome" -- not enough small intestin
Contact: Les Lang
University of North Carolina School of Medicine