Inhibition of attaching and effacing lesion formation following enteropathogenic Escherichia coli and Shiga toxin-producing E-coli infection

Enteropathogenic Escherichia coli (EPEC) and Shiga toxin-producing E. coli (STEC) induce cytoskeletal changes in infected epithelial cells. To further characterize host cytosolic responses to infection, a series of specific c ell-signaling inhibitors were employed. Initial bacterial adhesion to HEp-2 epithelial cells was not reduced, whereas alpha -actinin accumulation in i nfected cells was blocked by a phosphoinositide-specific phospholipase C in hibitor (ET-18-OCH3), phosphoinositide 3-kinase inhibitors (wortmannin and LY294002), and a 5-lipoxygenase inhibitor, nordihydroguaretic acid. A cyclo oxygenase-2 inhibitor (NS-398), however, did not block a.-actinin reorganiz ation in response to EPEC and STEC infections. Understanding signal transdu ction responses to enteric pathogens could provide the basis for the develo pment of novel therapeutic strategies.