1887

Abstract

The hage-hock rotein (Psp) system is believed to manage membrane stress in all and has recently emerged as being important for virulence in several pathogenic species of this phylum. The core of the Psp system consists of the operon and the distantly located gene. In serovar Typhimurium (. Typhimurium), it has recently been reported that PspA is essential for systemic infection of mice, but only in NRAMP1 mice, signifying that attenuation is related to coping with divalent cation starvation in the intracellular environment. In the present study, we investigated the contribution of individual genes to virulence of . Typhimurium. Interestingly, deletion of the whole set of genes caused attenuation in both NRAMP1 and NRAMP1 mice, indicating that one or more of the genes contribute to virulence independently of NRAMP1 expression in the host. Investigations of single gene mutants showed that knock out of reduced virulence in both types of mice, while deletion of only caused attenuation in NRAMP1 mice, and deletion of had a minor effect in NRAMP1 mice, while deletions of either or did not affect virulence. Experiments addressed at elucidating the role of PspB in virulence revealed that PspB is dispensable for uptake to and intracellular replication in cultured macrophages and resistance to complement-induced killing. Furthermore, the Psp system of Typhimurium was dispensable during pIV-induced secretin stress. In conclusion, our results demonstrate that removal of PspB reduces virulence in . Typhimurium independently of host NRAMP1 expression, demonstrating that PspB has roles in intra-host survival distinct from the reported contributions of PspA.

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2014-06-01
2024-04-24
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