Where are we on worms?

Abstract

There is something about living in an industrialized country that dramatically increases the risk of acquiring inflammatory bowel disease (IBD). Loss of routine exposure to parasitic worms (helminths), due to modern highly hygienic life styles, likely contributes to this risk. This article reviews current understanding on how helminths influence intestinal inflammation and mucosal immune responses. IBD emerges in populations as regions develop socioeconomically and lose exposure to previously ubiquitous helminthic infections. Helminthic infections provided strong selective pressure for the dissemination of gene variants, many of which predispose to development of IBD. In animal models of IBD, helminth colonization suppresses intestinal inflammation through multiple mechanisms including induction of innate and adaptive regulatory circuits. Trials using helminths like hookworm (Necator americanus) or porcine whipworm (Trichuris suis) show that they are safe and may be effective therapies for the control of the aberrant intestinal inflammation seen in Crohn's disease and ulcerative colitis. Evidence is accumulating that highly hygienic living conditions create risk for developing immune-mediated disease such as IBD. To live in their host, helminths have developed the ability to activate cells of innate and adaptive immunity that suppress inflammation. Therapeutic trials using helminths are in progress.