An anti-inflammatory therapy utilizing proteins called type 1 interferon IFN-alpha and IFN-beta (IFN-á/â) has been shown by researchers at the University of California, San Diego (UCSD) School of Medicine and their colleagues in Japan and Israel to offer relief in mouse models of Crohns disease and ulcerative colitis, the two major forms of the painful, chronic condition called inflammatory bowel disease (IBD) that affects nearly 1 million Americans.
Published in the March 2005 issue of the Journal of Clinical Investigation (JCI), the study provides the first description of the molecular mechanism by which IFN-á/â inhibits the severity of colitis and maintains intestinal homeostasis, or the "constant state" of the gut, by suppressing pro-inflammatory activity by the immune system macrophages. "Although IFN-á/â therapy has been tried in recent clinical trials, along with other anti-inflammatory treatments, researchers have not understood how or why IFN-á/â might work as an IBD treatment," said Eyal Raz, M.D., UCSD professor of medicine and the studys senior author. "Our study describes how activated IFN-á/â plays a protective role in colonic inflammation."
The studys first author, Kyoko Katakura, M.D, Department of Medicine II, Fukushima, Japan, added that the teams results point to an important protective and potential therapeutic role for IFN-á/â. In an accompanying Commentary in the March issue of JCI, German researchers Stefan Wirtz and Markus F. Neurath noted that the results "suggest that strategies to modulate innate immunity may be of therapeutic value." They added that "It is astonishing to realize that in spite of the existence of clinical trials on the use of IFN-á/â in the treatment of UC (ulcerative colitis), there is only very limited information about their expression and biological function in the immune system of the gut."
Sue Pondrom | EurekAlert!
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