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(The FASEB Journal. 2000;14:1848-1855.)
© 2000 FASEB

Does the failure to acquire helminthic parasites predispose to Crohn’s disease?

DAVID E. ELLIOTT*1, JOE F. URBAN, JR.{dagger}, CURTIS K. ARGO* and JOEL V. WEINSTOCK*1

* Department of Internal Medicine, Division of Gastroenterology/Hepatology, University of Iowa, Iowa City, Iowa 52242, USA; and
{dagger} The Immunology and Disease Resistance Laboratory, U.S. Department of Agriculture, Beltsville, Maryland 20705, USA

1Correspondence: Division of Gastroenterology/Hepatology, University Hospital (4611 JCP), 200 Hawkins Dr., Iowa City, IA 52242-1009, USA. E-mail: david-elliott@uiowa.edu or joel-weinstock{at}uiowa.edu

Two polarized patterns (Th1 and Th2) of cytokines regulate inflammatory responses. Each cytokine pattern inhibits production of the opposing pattern. Lymphocytes from inflamed intestine due to Crohn’s disease secrete a Th1 pattern of cytokines. Crohn’s disease is most prevalent in highly industrialized countries with temperate climates. It occurs rarely in tropical third world countries with poor sanitation. We propose that exposure to an environmental agent predisposes individuals to Crohn’s disease. Parasitic worms (helminths) are common in tropical climates and in populations subject to crowding and poor sanitation. Children are most subject to helminthic colonization. Many helminths live within or migrate through the human gut where they interact with the mucosal immune system. The host mounts a mucosal response that includes Th2 cytokine production limiting helminthic colonization. Helminths and their eggs probably are the most potent stimulators of mucosal Th2 responses. The Th2 response provoked by parasitic worms can modulate immune reactions to unrelated parasitic, bacterial, and viral infections. Many people in developed countries now live in increasingly hygienic environments, avoiding exposure to helminths. Perhaps failure to acquire these parasites and experience mucosal Th2 conditioning predisposes to Crohn’s disease, which is an overly active Th1 inflammation.—Elliott, D. E., Urban, J. F., Jr., Argo, C. K., Weinstock, J. V.


Key Words: ulcerative colitis • helminths • Th1/Th2 response • CD




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