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Novel pathogenetic mechanism in a clinical isolate of Yersinia enterocolitica KU14

Yoshinori Sato1, Kenichi Kaneko, Takeshi Sasahara

  • 1Environmental Infectious Disease, Graduate School of Medical Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara-shi, Kanagawa 228-8555, Japan.

Journal of Microbiology (Seoul, Korea)
|March 24, 2006
PubMed

Insights

Yersinia enterocolitica KU14, lacking the pYV plasmid, exhibits enhanced intracellular growth in macrophages. This growth is mediated by lipid rafts, suggesting a novel infection mechanism for this pathogen.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogen-host interactions

Background:

  • Yersinia enterocolitica is a significant cause of bacterial gastroenteritis.
  • The pYV virulence plasmid is typically associated with Yersinia pathogenicity.
  • Previous work showed Y. enterocolitica KU14, lacking pYV, can still cause infection.

Purpose of the Study:

  • To investigate the mechanism behind the intracellular survival and growth of Y. enterocolitica KU14 in macrophages.
  • To determine the role of lipid rafts in Y. enterocolitica KU14 infection.

Main Methods:

  • Macrophage cell culture and infection assays.
  • Comparison of Y. enterocolitica strains with and without the pYV plasmid.
  • Treatment with beta-cyclodextrin to disrupt lipid rafts.

Main Results:

  • Y. enterocolitica KU14 did not induce macrophage death, unlike pYV-harboring strains.
  • KU14 demonstrated significantly greater intracellular growth within macrophages compared to a non-plasmid strain.
  • Disruption of lipid rafts with beta-cyclodextrin markedly reduced intracellular KU14 growth.

Conclusions:

  • The pYV plasmid is not essential for Y. enterocolitica to infect macrophages.
  • Enhanced intracellular growth of Y. enterocolitica KU14 is dependent on lipid raft-mediated mechanisms.
  • Lipid rafts represent a potential target for therapeutic intervention against Yersinia infections.

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