The inflammatory response is an integral part of host defense against enterohemorrhagic Escherichia coli (EHEC)
infection and also contributes to disease pathology. In this article we explore the factors leading to
inflammation during EHEC
infection and the mechanisms EHEC and other attaching and effacing (A/E) pathogens have evolved to suppress inflammatory signaling. EHEC stimulates an inflammatory response in the intestine through host recognition of bacterial components such as
flagellin and
lipopolysaccharide. In addition, the activity of
Shiga toxin and some
type III secretion system effectors leads to increased tissue
inflammation. Various
infection models of EHEC and other A/E pathogens 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. The inflammatory response of infected enterocytes is counterbalanced by the activity of
type III secretion system effectors such as NleE and NleC that modify and inhibit components of the signaling pathways that lead to proinflammatory
cytokine production. Overall, A/E pathogens have taught us that innate mucosal immune responses in the gastrointestinal tract during
infection with A/E pathogens 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.