1887

Abstract

Melioidosis is a severe infectious disease of animals and humans caused by the Gram-negative intracellular pathogen . An Inv/Mxi-Spa-like type III protein secretion apparatus, encoded by the locus, facilitates bacterial invasion of epithelial cells, escape from endocytic vesicles and intracellular survival. This study investigated the role of the Bsa type III secretion system in the pathogenesis of melioidosis in murine models. mutants, lacking a component of the translocation apparatus, were found to be significantly attenuated following intraperitoneal or intranasal challenge of BALB/c mice. Furthermore, a mutant was attenuated in C57BL/6 IL-12 p40 mice, which are highly susceptible to infection. Mutation of impaired bacterial replication in the liver and spleen of BALB/c mice in the early stages of infection. mutants lacking either the type III secreted guanine nucleotide exchange factor BopE or the putative effectors BopA or BopB exhibited varying degrees of attenuation, with mutations in and causing a significant delay in median time to death. This indicates that -encoded type III secreted proteins may act in concert to determine the outcome of infection in mice. Mice inoculated with the mutant were partially protected against subsequent challenge with wild-type . However, immunization of mice with purified BipD protein was not protective.

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2004-08-01
2019-10-20
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