[Mechanism of A/E lesion formation produced by enterohemorrhagic Escherichia coli: O157--role of EspB, Tir and cortactin].

Enterohemorrhagic Escherichia coli(EHEC) belongs to a family of pathogens which cause attaching and effacing(A/E) lesion on target cells. The following event is the alteration of the host intestinal cell cytoskeleton to form a pedestal-like structure. As a result of some recent breakthrough discoveries, EHEC injects effector proteins, EspB and Tir, into the host cells by type III secretion machinery and they modify cellular function and lead the signaling events by its direct binding with cytoskeletal proteins, alpha-catenin and talin. Cortactin is also accumulated to adherent site and involved in EHEC-induced A/E lesion. As a result of those interaction between bacterial effector proteins and host cytoskeletal proteins, EHEC can trigger the rearrangement of the host cell's actin cytoskeleton and induce the A/E lesion.