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Review
. 2010 Mar;45(3):266-76.
doi: 10.1007/s00535-009-0191-y.

The role of infection in the aetiology of inflammatory bowel disease

Richard Hansen  1 , John M Thomson, Emad M El-Omar, Georgina L Hold
Affiliations
Review

The role of infection in the aetiology of inflammatory bowel disease

Richard Hansen et al. J Gastroenterol. 2010 Mar.

Abstract

We have greatly increased our understanding of the genetics of inflammatory bowel disease (IBD) in the last decade; however, migrant studies highlight the importance of environment in disease risk. The possibility that IBD is an infection has been debated since the first description of Crohn's disease. Mycobacterium avium paratuberculosis was the first organism to be suggested as an IBD pathogen, and it has been argued that it fulfils Koch's postulates and could be designated the cause of Crohn's disease. Other organisms have been postulated as possible IBD pathogens, including various Helicobacter species, one of which has been identified in primate colitis;others are widely used in animal models of IBD. Adherent invasive Escherichia coli appear specific to ileal Crohn's disease and have been shown to induce the release of TNF-alpha, a key cytokine in IBD inflammation. The aim of this article is to give a concise overview of the infections postulated as being relevant to the onset of IBD. We will also briefly cover the immunology underpinning IBD, in addition to reviewing current knowledge regarding other microorganisms that are associated with modifying the risk of developing IBD. It may be that infectious organisms have an orchestrator role in the development of dysbiosis and subsequently IBD.

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Figures

Fig. 1
Fig. 1
T cell balance between intestinal inflammation and health. IBD immunology centres on an imbalance between pro-inflammatory effector T cells typified by TH17 and regulatory T cells (TReg). The differentiation of TH17 is dependent on IL-23, and this cell lineage is responsible for the key pro-inflammatory cytokine IL-17. The development of regulatory T cells is controlled by FOXP3, and the anti-inflammatory cytokines released include IL-10 and IL-35 along with TGF-β, which can be pro-inflammatory or anti-inflammatory
Fig. 2
Fig. 2
Potential pathological cascade in inflammatory bowel disease. An underlying genetic susceptibility leads to the development of bacterial population shifts within the gastrointestinal tract to the detriment of the host (dysbiosis) after a trigger event. This leads to chronic intestinal inflammation and inflammatory bowel disease
See this image and copyright information in PMC

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