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Related Experiment Video

Updated: Jun 2, 2026

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
07:10

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

Global changes in Staphylococcus aureus gene expression in human blood.

Natalia Malachowa1, Adeline R Whitney, Scott D Kobayashi

  • 1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America.

Plos One
|April 29, 2011
PubMed
Summary

Staphylococcus aureus USA300 up-regulates gamma-hemolysin in human blood, impacting neutrophil lysis and bloodstream infection models. Functional redundancy among leukotoxins influences virulence.

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Staphylococcus aureus Growth using Human Hemoglobin as an Iron Source
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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Staphylococcus aureus, particularly the USA300 strain, is a major cause of bloodstream infections globally.
  • The molecular mechanisms by which S. aureus survives in human blood and causes metastasis are not fully understood.

Purpose of the Study:

  • To investigate the USA300 transcriptome in human blood, serum, and TSB to identify virulence factors.
  • To determine the role of gamma-hemolysin (hlgABC) in S. aureus USA300 virulence, neutrophil lysis, and host survival.

Main Methods:

  • Transcriptome analysis of USA300 cultured in human blood, serum, and TSB.
  • Assessing neutrophil pore formation and lysis using wild-type and hlgABC-deletion strains.
  • Evaluating bacterial virulence in mouse bacteremia and skin infection models.

Main Results:

  • Genes for cytolytic toxins, including hlgABC, were significantly upregulated in human blood.
  • The hlgABC deletion mutant showed reduced neutrophil lysis and modestly reduced mortality in a mouse bacteremia model.
  • Functional redundancy was observed among two-component leukotoxins, suggesting a collective role in virulence.

Conclusions:

  • Gamma-hemolysin expression is induced by human blood and contributes to S. aureus USA300 virulence, particularly neutrophil lysis.
  • Leukotoxin redundancy may explain the limited contribution of individual toxins to immune evasion and overall virulence.
  • Specific growth conditions are critical for leukotoxin expression and subsequent virulence.