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Authors’ contributions YC participated in the bacteriocin analysis and construction

of the null GSI-IX mw alleles of the fliC and flhA genes. DC conceived the study, participated in its design, and corrected the manuscript. All authors read and approved the final manuscript.”
“Background The inflammatory bowel diseases (IBD), Crohn disease and ulcerative colitis, are relatively common chronic disorders considered to develop due to an aberrant immune response to intestinal microbes in a genetically susceptible host [1]. Human data and murine models both implicate the involvement of luminal bacteria in IBD pathogenesis. For example, inflammation is induced BCKDHA by direct delivery of fecal material into non-inflamed bowel loops in susceptible individuals [2] and diversion of feces results in distal improvement in mucosal inflammation [3]. In addition, most of the genes associated with susceptibility to IBD, including NOD2/CARD15, Atg16L1 and IRGM encode proteins involved in host-microbial interactions [4]. Further support for the involvement of microbes in the pathogenesis of IBD is based on the observation that colitis does not occur in most gene knock-out models of IBD when animals are reared in germ-free conditions [5, 6]. Recent advances in molecular techniques have identified a reduction in the phyla Firmicutes and Bacteroidetes in IBD patients [7]. Although several organisms have been proposed as a cause of IBD, there is still no compelling evidence that any one specific microbe is the etiologic agent.