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An Inv/Mxi-Spa-like type III protein secretion system in Burkholderia pseudomallei modulates intracellular behaviour

Mark P Stevens1, Michael W Wood, Lowrie A Taylor

  • 1Division of Environmental Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, UK.

Molecular Microbiology
|November 2, 2002
PubMed

Insights

The Bsa type III secretion system is crucial for Burkholderia pseudomallei to survive inside host cells. This system enables the bacteria to escape vacuoles, spread between cells, and cause melioidosis.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Cell Biology

Background:

  • Melioidosis is a severe infectious disease caused by Burkholderia pseudomallei, a facultative intracellular pathogen.
  • B. pseudomallei invades host cells, escapes into the cytoplasm, and utilizes actin-based motility for cell-to-cell spread, contributing to virulence.
  • A type III protein secretion apparatus (Bsa) in B. pseudomallei is homologous to systems in Salmonella and Shigella, suggesting a role in pathogenesis.

Purpose of the Study:

  • To investigate the role of the Bsa type III secretion system in the interaction between B. pseudomallei and host cells.
  • To determine the Bsa system's contribution to bacterial intracellular survival, vacuole escape, and cell-to-cell spread.

Main Methods:

  • Construction and characterization of B. pseudomallei mutant strains lacking components of the Bsa secretion and translocation apparatus.
  • Analysis of bacterial behavior within J774.2 murine macrophage-like cells, including replication, vacuole escape, and actin-based motility.

Main Results:

  • Mutant strains lacking Bsa components showed reduced replication in macrophages.
  • These mutants were unable to escape from endocytic vacuoles.
  • The formation of membrane protrusions and actin tails, essential for cell-to-cell spread, was completely absent in the mutant strains.

Conclusions:

  • The Bsa type III secretion system is essential for B. pseudomallei's intracellular survival and pathogenesis.
  • The Bsa system mediates vacuole escape and actin-based motility, facilitating host cell invasion and spread.
  • Targeting the Bsa system could be a potential strategy for treating melioidosis.

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