Molecular Pathogenesis ofShigellaspp.: Controlling Host Cell Signaling, Invasion, and Death by Type III Secretion

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Abstract
SUMMARY: Shigellaspp. are gram-negative pathogenic bacteria that evolved from harmless enterobacterial relatives and may cause devastating diarrhea upon ingestion. Research performed over the last 25 years revealed that a type III secretion system (T3SS) encoded on a large plasmid is a key virulence factor ofShigella flexneri. The T3SS determines the interactions ofS. flexneriwith intestinal cells by consecutively translocating two sets of effector proteins into the target cells. Thus,S. flexnericontrols invasion into EC, intra- and intercellular spread, macrophage cell death, as well as host inflammatory responses. Some of the translocated effector proteins show novel biochemical activities by which they intercept host cell signal transduction pathways. An understanding of the molecular mechanisms underlyingShigellapathogenesis will foster the development of a safe and efficient vaccine, which, in parallel with improved hygiene, should curb infections by this widespread pathogen.