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PLoS Pathog. 2014 Aug 7;10(8):e1004306. doi: 10.1371/journal.ppat.1004306. eCollection 2014 Aug.

The Vi capsular polysaccharide enables Salmonella enterica serovar typhi to evade microbe-guided neutrophil chemotaxis.

Author information

1
Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, California, United States of America.
2
Department of Biomedical Engineering, University of California, Davis, Davis, California, United States of America.

Abstract

Salmonella enterica serovar Typhi (S. Typhi) causes typhoid fever, a disseminated infection, while the closely related pathogen S. enterica serovar Typhimurium (S. Typhimurium) is associated with a localized gastroenteritis in humans. Here we investigated whether both pathogens differ in the chemotactic response they induce in neutrophils using a single-cell experimental approach. Surprisingly, neutrophils extended chemotactic pseudopodia toward Escherichia coli and S. Typhimurium, but not toward S. Typhi. Bacterial-guided chemotaxis was dependent on the presence of complement component 5a (C5a) and C5a receptor (C5aR). Deletion of S. Typhi capsule biosynthesis genes markedly enhanced the chemotactic response of neutrophils in vitro. Furthermore, deletion of capsule biosynthesis genes heightened the association of S. Typhi with neutrophils in vivo through a C5aR-dependent mechanism. Collectively, these data suggest that expression of the virulence-associated (Vi) capsular polysaccharide of S. Typhi obstructs bacterial-guided neutrophil chemotaxis.

Comment in

PMID:
25101794
PMCID:
PMC4125291
DOI:
10.1371/journal.ppat.1004306
[Indexed for MEDLINE]
Free PMC Article

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