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The importance of gut microbiota in mediating the effect of NOD2 defects in inflammatory bowel disease
  1. Gerhard Rogler
  1. Correspondence to Professor Dr G. Rogler, Division of Gastroenterology and Hepatology, Department of Internal Medicine, University-Hospital of Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland

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It is well accepted that genetic factors contribute to the pathogenesis of Crohn's disease. Susceptibility genes have been identified; however, the exact mechanisms of how those risk genes contribute to the pathogenesis of Crohn's disease still remain to be elucidated. Therefore, insights such as those provided by Barreau and co-workers from the group of Jean-Pierre Hugot in this issue of Gut1 (see page 207) are important and helpful.

The proof of the ‘genetic susceptibility concept’ for Crohn's disease was achieved in 2001 by Hugot and others by the finding that single nucleotide polypmorphisms (SNPs) in the NOD2 gene are significantly associated with the risk of developing Crohn's disease.2–4 About 20–40% of all patients in Europe and North America—depending on the genetic background—carry variants of NOD2 in contrast to 10–15% in the healthy population. Three major NOD2 genetic variants have been associated with Crohn's disease in Caucasians in several independent studies. In contrast, NOD2 variants are irrelevant in the Asian population and do not play a role in the pathogenesis of Crohn's disease in Japan or China.5 6

The function of Nod2 has been intensively investigated since then. Muramyl dipeptide (MurNAc-l-Ala-d-isoGln, MDP), a component of the bacterial wall derived from peptidoglycan, …

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  • Competing interests None.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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