Salmonella SPI-2 Type III Secretion System Effectors: Molecular Mechanisms And Physiological Consequences

Abstract

Serovars of Salmonella enterica cause both gastrointestinal and systemic diseases in a broad range of mammalian hosts, including humans. Salmonella virulence depends in part on its pathogenicity island 2 type III secretion system (SPI-2 T3SS), which is required to translocate at least 28 effector proteins from vacuolar-resident bacteria into host cells. Comparative genomic analysis reveals that all serovars encode a subset of "core" effectors, suggesting that they are critical for virulence in different hosts. An additional subset of effectors is found sporadically throughout different serovars, and several inhibit activation of the innate immune system. In this Review, we summarize the biochemical activities, host cell interaction partners, and physiological functions of SPI-2 T3SS effectors in the context of the selective pressures encountered by S. enterica in vivo. We also consider some of the remaining challenges to achieve a unified understanding of how effector activities work together to promote Salmonella virulence.

Keywords: SPI-2; Salmonella; bacterial pathogen; effector; pathogenicity island; type III secretion system; virulence.