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Inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) or ulcerative colitis (UC) comprise the two most common forms of intestinal inflammation characterised by a chronic relapsing disease course. The aetiology of both disorders has still not yet been identified. Whereas it has been elegantly demonstrated in many studies in the last years that genetic factors are crucially involved, other so-called environmental factors are much less well defined.1 In recent years evidence was accumulating that the gut microbiota and its manipulation might constitute one of those relevant ‘environmental’ factors. Trillions of microbes compose the intestinal microbiota of healthy individuals and several studies have demonstrated in the past that IBD patients exhibit a pronounced dysbiosis. It remains, however, speculative whether observed changes are causally involved in IBD pathogenesis or reflect simply epiphenomena due to inflammation.2
Whereas several clinical aspects strongly support a role for intestinal bacteria in CD such as improvement of inflammation after diversion of the faecal stream or improvement of disease during antibiotic therapy, similar observations are mostly not available for UC. However, other aspects are suggesting a role for bacteria in the pathogenesis of UC as, for example, abnormal mucosal secretion of IgG antibodies …
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