Pathological interactions of bacteria and toxins with the gastrointestinal epithelial tight junctions and/or the zonula adherens: An update

Communication between bacteria and the gastrointestinal tight junctions (TJs) and zonula adherens is examined. Bacterial epithelial Us "crosstalk" can be mediated by many virulence factors, mainly secreted toxins, or can be induced by direct contact of the pathogen with epithelial membrane. Moreover, there are several mechanisms by which bacteria may act on gastrointestinal TJs. First, bacteria can act indirectely at the Us level by inducing cell transepithelial migration. More particularly, neutrophil or dendritic cells can cross the epithelium by a paracellular pathway. Secondly, bacteria and/or toxins can trigger actin cytoskeleton reorganization (depolymerization or hyperpolymerization). Thirdly, some enteric pathogens are susceptible to act on Us by activation of cellular signal transduction. Finally, cleavage or modification of TJs proteins can be used by bacteria. New therapeutic strategies may result from a deeper knowledge of the cellular and molecular processes induced by bacteria at the TJ level. Moreover, studies of action of the different bacterial virulence factors on the molecules comprising the Us and zonula adherens allow us an interesting approach on our understanding of TJ complex regulation.