EspF U, a type III-translocated effector of actin assembly, fosters epithelial association and late-stage intestinal colonization by E. coli O157:H7

Abstract

Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 induces filamentous actin-rich 'pedestals' on intestinal epithelial cells. Pedestal formation in vitro requires translocation of bacterial effectors into the host cell, including Tir, an EHEC receptor, and EspFu, which increases the efficiency of actin assembly initiated by Tir. While inactivation of espFu does not alter colonization in two reservoir hosts, we utilized two disease models to explore the significance of EspFu-promoted actin pedestal formation. EHECΔespFu efficiently colonized the rabbit intestine during co-infection with wild-type EHEC, but co-infection studies on cultured cells suggested that EspFu produced by wild-type bacteria might have rescued the mutant. Significantly, EHECΔ espFu by itself was fully capable of establishing colonization at 2days post inoculation but unlike wild type, failed to expand in numbers in the caecum and colon by 7days. In the gnotobiotic piglet model, an espFu deletion mutant appeared to generate actin pedestals with lower efficiency than wild type. Furthermore, aggregates of the mutant occupied a significantly smaller area of the intestinal epithelial surface than those of the wild type. Together, these findings suggest that, after initial EHEC colonization of the intestinal surface, EspFu may stabilize bacterial association with the epithelial cytoskeleton and promote expansion beyond initial sites of infection. © 2007 The Authors Journal compilation © 2007 Blackwell Publishing Ltd.