Understanding inflammatory bowel disease

The inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis, are immune-mediated disorders that arise in genetically susceptible individuals from a breakdown in the regulatory constraints on mucosal immune responses to enteric bacteria. Heterogeneity between and within these inflammatory diseases seems likely, with disparate underlying defects linked to a similar pathophysiological outcome. Critical to the pathogenesis of these conditions is an understanding of the mechanisms by which the mucosal immune system senses the environment. Regulation of immune reactivity to enteric antigens is under genetic control; genes which code for proteins involved in immune interactions with environmental bacteria predispose to CD and it seems likely that additional genes regulating immune interpretation of the environment will be identified as risk factors for IBD. Traditionally, drug therapy for IBD has been directed at suppression of the host immuno-inflammatory response, but therapeutic manipulation of the enteric microflora is emerging as an adjunctive option. However, full realisation of this strategy requires better characterisation of the commensal enteric bacteria and their interactions with the host. Since most of the enteric bacteria are still uncultureable, modern molecular techniques will be required to complement conventional microbiology. Notwithstanding the scientific obstacles, therapeutic modification of the gut flora with functional foods promises to empower patients and enable them to achieve a greater sense of control in the management of their illness.