Immunity to Enteropathogenic Escherichia coli

Enteropathogenic Escherichia coli (EPEC) is a highly evolved pathogen that has adapted to survive and cause disease in diverse environmental niches. The inflammatory response is an integral part of host defense against gut pathogens but also contributes to disease pathology. In this article, we explore the factors leading to inflammation during EPEC infection and the mechanisms EPEC and other attaching and effacing (A/E) pathogens have evolved to suppress inflammatory signaling. Infection with EPEC stimulates a rapid host inflammatory response via recognition of flagellin and LPS. Infection models of EPEC have revealed many of the immune factors that mediate this response. In particular, the outcome of infection is greatly influenced by the ability of an infected epithelial cell to mount an effective host inflammatory response. In order to counterbalance the inflammatory response, the bacteria inject effector proteins that inhibit inflammatory cytokine production, allowing the bacteria command exquisite control over the host to coordinate a successful infection strategy and cause disease. Overall, innate mucosal immune responses in the gastrointestinal tract during infection with EPEC are highly complex and ultimate clearance of the pathogen depends on multiple factors including inflammatory mediators, bacterial burden, and the function and integrity of resident intestinal epithelial cells.