Salmonella multimutants enable efficient identification of SPI-2 effector protein function in gut inflammation and systemic colonization.

ABSTRACT: Salmonella enterica spp. rely on translocation of effector proteins through the SPI-2 encoded type III secretion system (T3SS) to achieve pathogenesis. More than 30 effectors contribute to manipulation of host cells through diverse mechanisms, but interdependency or redundancy between effectors complicates the discovery of effector phenotypes using single mutant strains. Here, we engineer six mutant strains to be deficient in cohorts of SPI-2 effector proteins, as defined by their reported function. Using various animal models of infection, we show that three principle phenotypes define the functional contribution of the SPI-2 T3SS to infection. Multimutant strains deficient for intracellular replication, for manipulation of host cell defences, or for expression of virulence plasmid

SUBMITTER: Newson JPM 

PROVIDER: S-EPMC11661221 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature