Any pathogenic bacterial species must successfully replicate inside its host to ensure its own survival. Pathogenesis research has largely focused on “classical” virulence factors that enable the bacterium to manipulate host cell functions such as toxins or secretion machinery. In contrast, we have a very limited understanding of the metabolism of bacterial pathogens inside the host. In the case of enteric pathogens, this limited understanding likely stems from the fact that the contribution of intestinal commensal microbes (microbiota) has been neglected in the past. Recent advances in sequencing technology have allowed us to recognize that a complex ecosystem with extensive metabolic capabilities inhabits the large intestine. The focus of our research group is to determine the molecular mechanisms that shape the interaction between the host and the intestinal microbiota in particular when this interaction is perturbed during episodes of intestinal inflammation. A better understanding of these complex interactions will likely have a significant impact on a variety of inflammatory disease such as irritable bowel syndrome, IBD, metabolic syndrome, and infectious inflammatory diarrhea. The overarching principle for our hypotheses is that inflammation generates a peculiar nutritional environment in the gut: Specific compounds, e.g. electron acceptors, are generated as byproducts of the host inflammatory response and utilization of these compounds enhances the selective outgrowth of certain bacterial species, ultimately leading to dysbiosis. We have two main focuses in our research: Interactions among the host, the intestinal microbiota, and enteric pathogens, particularly during episodes of intestinal inflammation. The mechanisms of microbiota changes in the inflamed intestine in the absence of a bacterial pathogen.