Mediators and Outcomes of Bacteria-epithelial Cell Interactions

Intestinal mucosal surfaces are in continuous contact with heterogeneous populations of commensal microorganisms, which collectively make up the intestinal microbiota. Historically, the barrier function of intestinal epithelial cells (IEC) has been considered to be important in preventing or limiting the interaction of non-invasive bacteria from making contact with, and activating the mucosal immune system, and therefore maintaining immune (oral) tolerance to commensal bacteria. More recent investigations suggests that IEC may also play a role in sensing the external environment and communicating this information to the local immune system to affect appropriate responses. In this review the basis of IEC recognition of microorganisms and how disruption or breakdown in the interaction between IEC and the commensal microbiota are thought to underlie the development of chronic intestinal inflammation are discussed. In particular, the function of the cell surface pattern recognition receptors (PRR), Toll-like receptors, and the cytosolic nucleotide binding site plus leucine-rich repeat protein, NOD2, in IEC and the outcome of the triggering of these PRRs for IEC function are discussed.