Inflammatory Bowel Disease and Trichuris muris

Abstract

Inflammatory bowel disease (IBD) is a group of idiopathic chronic relapsing inflammatory conditions of the gastrointestinal tract. The precise etiology of IBD is unknown, although it is clearly multifactorial resulting from interplay of genetic, environmental and immunological factors. Epidemiological studies show that the incidence of IBD and other autoimmune disorders is low in the developing countries and more in the developed countries. Evidence suggests that therapeutic administration of helminth can reduce the symptoms of IBD in both animal models and man. However, one study show the rat tapeworm Hymenolepis diminuta infection results in significant exacerbation of oxazolone induced colitis in mice (Hunter et al., 2007). The mechanisms by which helminths interact with the gut immune system in IBD-susceptible hosts, particularly their effect on the onset and progression of colitis are poorly understood. To address this we have investigated the interaction between Trichuris muris and the mdr1a (-/-) mouse model, which lacks the epithelial barrier protein, p-glycoprotein and slowly develops a spontaneous colitis in the presence of a normal gut flora.