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Yersinia pestis two-component gene regulatory systems promote survival in human neutrophils

Jason L O'Loughlin1, Justin L Spinner, Scott A Minnich

  • 1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA.

Infection and Immunity
|November 26, 2009
PubMed

Insights

Yersinia pestis evades human immune cells by modifying its lipid A, a key component of its outer membrane. This modification, regulated by PhoPQ, enhances bacterial resistance to neutrophil antimicrobial defenses.

Area of Science:

  • Immunology
  • Microbiology
  • Bacterial Pathogenesis

Background:

  • Human polymorphonuclear leukocytes (PMNs) are crucial for innate immunity against bacteria.
  • Yersinia pestis evades PMN killing through incompletely understood mechanisms.
  • Understanding Y. pestis survival within neutrophils is vital for combating infections.

Purpose of the Study:

  • To identify Yersinia pestis genetic factors involved in intracellular survival within human neutrophils.
  • To elucidate the molecular mechanisms underlying Y. pestis resistance to PMN-mediated killing.

Main Methods:

  • Systematic inactivation of 25 two-component regulatory systems (TCSs) in Y. pestis.
  • Assessment of mutant strain susceptibility to human PMN granule extracts and antimicrobial peptides.
  • Analysis of Y. pestis strains deficient in specific PhoP-regulated genes (ugd, pmrK).

Main Results:

  • Five TCS mutant strains (PhoPQ, KdpED, CheY, CvgSY, CpxRA) showed altered survival in PMNs.
  • Y. pestis deficient in PhoPQ (DeltaphoPQ) exhibited sensitivity to neutrophil antimicrobial peptides and proteases.
  • DeltaphoPQ demonstrated significantly reduced intracellular survival in human PMNs.
  • 4-amino-4-deoxy-l-arabinose modification of lipid A was identified as a key resistance mechanism.

Conclusions:

  • The PhoPQ TCS is critical for Yersinia pestis resistance to human neutrophil defenses.
  • Lipid A modification with 4-amino-4-deoxy-l-arabinose is a major virulence factor for Y. pestis survival in neutrophils.
  • This study reveals novel insights into Y. pestis immune evasion strategies.

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