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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

Insights into mechanisms used by Staphylococcus aureus to avoid destruction by human neutrophils

Jovanka M Voyich1, Kevin R Braughton, Daniel E Sturdevant

  • 1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, Hamilton, MT 59840, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|September 9, 2005
PubMed

Insights

Community-acquired Staphylococcus aureus strains evade immune cells more effectively than hospital-acquired strains. These virulent bacteria utilize specific gene transcription programs to resist killing by polymorphonuclear leukocytes (PMNs), contributing to infection survival.

Area of Science:

  • Microbiology and Immunology
  • Infectious Diseases
  • Bacterial Pathogenesis

Background:

  • Polymorphonuclear leukocytes (PMNs), or neutrophils, are crucial for innate immunity against bacterial infections.
  • Pathogens like Staphylococcus aureus can evade destruction by PMNs, leading to persistent human infections.
  • The molecular mechanisms by which bacteria circumvent host immune defenses are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms of Staphylococcus aureus pathogenesis and its interaction with PMNs.
  • To compare the virulence and immune evasion strategies of community-acquired (CA) versus hospital-acquired S. aureus strains.
  • To identify bacterial genes and transcriptional responses involved in evading innate host defense.

Main Methods:

  • Utilized mouse models to assess the virulence of different S. aureus strains (CA and hospital-acquired).
  • Analyzed bacterial interactions with human PMNs, including phagocytosis, reactive oxygen species production, and resistance to killing.
  • Performed microarray analysis to identify global gene expression changes in S. aureus during neutrophil phagocytosis.

Main Results:

  • Community-acquired S. aureus strains (MW2, MnCop) were more virulent and caused greater organ pathology than hospital-acquired strains (COL, MRSA252).
  • CA strains exhibited increased resistance to PMN killing and induced greater host cell lysis compared to hospital-acquired strains.
  • Phagocytosis triggered upregulation of S. aureus genes involved in capsule synthesis, regulation, oxidative stress, and virulence.
  • CA strains uniquely upregulated genes encoding virulence factors and hypothetical proteins during PMN phagocytosis.

Conclusions:

  • Specific gene transcription programs in S. aureus contribute to the evasion of innate host defense mechanisms, particularly PMNs.
  • Community-acquired strains possess distinct virulence and immune evasion strategies compared to hospital-acquired strains.
  • Understanding these bacterial mechanisms is critical for developing effective treatments against S. aureus infections.

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