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IBD is commonly considered as an exaggerated immune response to the microbiota in a genetically susceptible host. This statement recognises the central role of the enteric microbiota in the pathogenesis of IBD. Consistently, in animal models of IBD, inflammation is not observed in the absence of live bacteria and distinct members of the microbiota differ in their potential to trigger disease. Patients with IBD present substantial changes of their microbiota commonly described as dysbiosis.1–4 However, intestinal bacteria not only drive disease but quite the contrary, individual commensal members also dampen inflammatory responses and might thereby contribute to maintain host–microbial homeostasis (figure 1). This aspect seems of particular interest since it may provide the opportunity to develop therapeutic anti-inflammatory strategies.
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