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Yersinia pestis type III secretion system-dependent inhibition of human polymorphonuclear leukocyte function

Justin L Spinner1, Jennifer A Cundiff, Scott D Kobayashi

  • 1Department of Microbiology, Molecular Biology, and Biochemistry, University of Idaho, 209 Ag Biotech, Moscow, ID 83844, USA.

Infection and Immunity
|May 21, 2008
PubMed

Insights

Yersinia pestis uses its type III secretion system (TTSS) to survive outside human neutrophils (PMNs), but the bacteria are killed once inside, regardless of TTSS activity. This study clarifies bacterial fate during host defense against plague.

Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis

Background:

  • Human polymorphonuclear leukocytes (PMNs), or neutrophils, are critical for innate immunity against bacterial infections.
  • Yersinia pestis, the plague pathogen, can evade host defenses, but its interaction with neutrophils is not fully understood.
  • Neutrophils kill ingested bacteria using reactive oxygen species (ROS) and granule contents.

Purpose of the Study:

  • To investigate how Yersinia pestis interacts with human neutrophils.
  • To determine the role of the type III secretion system (TTSS) in Y. pestis survival and neutrophil responses.
  • To elucidate the mechanisms of bacterial killing by neutrophils.

Main Methods:

  • Differential fluorescence microscopy was used to assess Y. pestis phagocytosis by human PMNs.
  • The impact of Y. pestis TTSS expression on neutrophil ROS production was measured.
  • Gentamicin protection assays were employed to differentiate between extracellular and intracellular bacterial survival.

Main Results:

  • Y. pestis TTSS expression inhibits phagocytosis by human PMNs.
  • Y. pestis TTSS represses ROS production in human neutrophils, similar to other Yersinia species.
  • Intracellular Y. pestis, even TTSS-expressing strains, were eliminated by human PMNs.
  • Extracellular survival of Y. pestis was enhanced by TTSS expression.

Conclusions:

  • The Y. pestis TTSS promotes extracellular survival against human neutrophils.
  • Neutrophil-mediated killing of intracellular Y. pestis is independent of TTSS-mediated inhibition of ROS production.
  • TTSS primarily impacts bacterial fate during initial host-pathogen interaction at the extracellular level.

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