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Interaction of Yersinia pestis with macrophages: limitations in YopJ-dependent apoptosis

Ayelet Zauberman1, Sara Cohen, Emanuelle Mamroud

  • 1Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research, P.O. Box 19, Ness-Ziona, 74100, Israel.

Infection and Immunity
|May 23, 2006
PubMed

Insights

Yersinia pestis suppresses macrophage responses similarly to other Yersinia species, but its reduced effector translocation limits cell death. Enhancing effector delivery boosts Y. pestis cytotoxicity, potentially aiding early infection.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Enteropathogenic Yersinia strains use type III secretion system (T3SS) effectors to downregulate macrophage signaling.
  • YopJ/YopP is a key T3SS effector involved in Yersinia-mediated immune suppression.

Purpose of the Study:

  • To investigate the adverse effects of Yersinia pestis on macrophages.
  • To compare the immune evasion strategies of Y. pestis with other Yersinia species.

Main Methods:

  • Infection of macrophage cell lines (J774A.1, RAW264.7) and primary murine macrophages with Y. pestis strains.
  • Analysis of tumor necrosis factor alpha secretion, mitogen-activated protein kinase phosphorylation, NF-kappaB activation, and caspase activation.
  • Assessment of YopJ effector translocation efficiency and apoptosis induction.

Main Results:

  • Y. pestis, like enteropathogenic Yersinia, suppresses TNF-alpha secretion and MAPK phosphorylation in macrophages.
  • Y. pestis is less effective than Y. enterocolitica WA O:8 in activating caspases, suppressing NF-kappaB, and inducing apoptosis.
  • Lower YopJ effector translocation efficiency in Y. pestis contributes to these differences.
  • Enhanced effector translocation (high bacterial load, synchronized infection, exogenous YopJ/YopP overexpression) increases Y. pestis cytotoxicity.

Conclusions:

  • Y. pestis exhibits distinct immune modulation compared to highly virulent Yersinia strains due to differences in effector translocation.
  • The reduced ability of Y. pestis to induce macrophage apoptosis may facilitate its propagation during early infection stages.
  • Modulating YopJ/YopP effector function can alter Y. pestis virulence and cytotoxic potential.

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