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Quantifying the Cytotoxicity of Staphylococcus aureus Against Human Polymorphonuclear Leukocytes
12:27

Quantifying the Cytotoxicity of Staphylococcus aureus Against Human Polymorphonuclear Leukocytes

Published on: January 3, 2020

Rapid neutrophil destruction following phagocytosis of Staphylococcus aureus

Scott D Kobayashi1, Kevin R Braughton, Amy M Palazzolo-Ballance

  • 1Laboratory of Human Bacterial Pathogenesis, Research Technologies Section, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.

Journal of Innate Immunity
|July 1, 2010
PubMed

Insights

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) USA300 triggers rapid programmed necrosis in human neutrophils, contributing to its enhanced virulence. This neutrophil destruction mechanism differs from typical apoptosis or lysis by toxins.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) exhibits enhanced virulence.
  • Mechanisms of CA-MRSA virulence, including evasion of immune cells, are not fully understood.
  • Polymorphonuclear leukocytes (PMNs), or neutrophils, are critical immune cells for combating bacterial infections.

Purpose of the Study:

  • To investigate the mechanism of rapid PMN lysis following phagocytosis of the CA-MRSA strain USA300.
  • To differentiate the observed PMN death from standard apoptosis or phagocytosis-induced cell death.
  • To identify molecular changes in PMNs upon interaction with CA-MRSA.

Main Methods:

  • Phagocytosis assays using USA300 and human PMNs.
  • Morphological analysis of PMNs post-phagocytosis.
  • Transcriptomic analysis (microarray) of PMNs exposed to CA-MRSA and healthcare-associated MRSA strains.

Main Results:

  • Ingestion of USA300 by PMNs led to rapid lysis (within 6 hours).
  • PMN destruction exhibited characteristics of programmed necrosis, distinct from FAS-mediated apoptosis or phagocytosis-induced cell death.
  • Transcriptomic analysis revealed unique upregulation of calcium homeostasis-related transcripts in PMNs exposed to CA-MRSA.

Conclusions:

  • Neutrophil destruction induced by USA300 is a form of programmed necrosis, not direct lysis by toxins.
  • The ability of CA-MRSA to induce programmed necrosis in neutrophils is a significant factor in its enhanced virulence.
  • Understanding this mechanism provides insights into CA-MRSA pathogenesis and potential therapeutic targets.

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