The frequency of Crohn’s disease (CD) has increased substantially over the last 50 years. It is most prevalent in highly industrialised temperate regions. CD and ulcerative colitis (UC) are rare in less developed countries. This suggests that critical environmental factors affect the worldwide distribution of inflammatory bowel disease (IBD). The “IBD hygiene hypothesis” states that raising children in extremely hygienic environments negatively affects immune development which predisposes them to immunological diseases such as IBD.1 It is also postulated that the modern day lack of exposure to helminths due to our hygienic practices is an important environmental factor contributing to IBD. Until modern times, nearly all children and most adults harboured intestinal helminths. Helminths and the immune system of Homo sapiens co-evolved in close proximity over many 1000s of years. Helminths regulate their host’s immune system and prevent excessive inflammatory responses, which could underlie the mechanism of protection. Moreels and colleague2 now lend further support for this hypothesis by reporting in this issue of Gut that infection with the helminth Schistosoma mansoni protects rats from trinitrobenzene sulphonic acid (TNBS) induced colitis [see page 99].
Approximately two million people in the USA and Europe have CD or UC, which usually begins during the second to third decade of life. IBD probably results from an inappropriately vigorous immune response to contents of the intestinal lumen. Evidence supporting this contention includes the effectiveness of immune suppressants at controlling the disease and experimental data derived from mice prone to IBD because of defects in immune regulation.3 In most of these murine models, the inflammation is driven by T helper 1 (Th1) circuitry and by substances in the intestinal lumen.