Enteropathogenic Escherichia coli (EPEC) is a gram-negative bacterial patho
gen that adheres to human intestinal epithelial cells, resulting in watery,
persistent diarrhea. It subverts the host cell cytoskeleton, causing a rea
rrangement of cytoskeletal components into a characteristic pedestal struct
ure underneath adherent bacteria. In contrast to other intracellular pathog
ens that affect the actin cytoskeleton from inside the host cytoplasm, EPEC
remains extracellular and transmits signals through the host cell plasma m
embrane via direct injection of virulence factors by a "molecular syringe,"
the bacterial type III secretion system. One injected factor is Tir, which
functions as the plasma membrane receptor for EPEC adherence. Tir directly
links extracellular EPEC through the epithelial membrane and firmly anchor
s it to the host cell actin cytoskeleton, thereby initiating pedestal forma
tion. In addition to stimulating actin nucleation and polymerization in the
host cell, EPEC activates several other signaling pathways that lead to ti
ght junction disruption, inhibition of phagocytosis, altered ion secretion,
and immune responses. This review summarizes recent developments in our un
derstanding of EPEC pathogenesis and discusses similarities and differences
between EPEC pedestals, focal contacts, and Listeria monocytogenes actin t
ails.