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Articles in PresS, published online ahead of print November 13, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00049.2002
Submitted on February 11, 2002
Accepted on November 7, 2002
1 Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA, USA
2 Immunology Disease Resistance Laboratory, Animal and Natural Resources Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD, USA
* To whom correspondence should be addressed. E-mail: david-elliott{at}uiowa.edu.
Crohn's disease results from dysregulated Th1-type mucosal inflammation. Crohn's disease is rare in tropical countries, but prevalent in developed countries with temperate climates where its incidence rose after 1940. In contrast, exposure to helminthic parasites is common in tropical countries, but is rare in developed countries. Helminthic parasites induce immunomodulatory T cell responses in the host. We hypothesize that immunomodulatory responses due to helminths may attenuate excessive Th1-type inflammation. To test that hypothesis, mice were exposed to eggs of the helminth Schistosoma mansoni then challenged rectally with TNBS to induce colitis. Schistosome egg exposure attenuated TNBS colitis, and protected mice from lethal inflammation. Schistosome egg exposure diminished IFN
and enhanced IL4 production from 
CD3-stimulated spleen and mesenteric lymph node cells of TNBS-treated mice. Schistosome egg exposure decreased colonic IFN but increased IL10 mRNA expression in TNBS-treated mice. Intact Stat6 was required for attenuation of colitis. Exposure to helminths can decrease murine colonic inflammation.
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