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Staphylococcal Enterotoxin O Exhibits Cell Cycle Modulating Activity.

Elisabeth Hodille1, Ludmila Alekseeva2, Nadia Berkova3

  • 1International Center for Infectiology ResearchLyon, France; CNRS UMR5308, Inserm U1111, Ecole Normale Supérieure de Lyon - Université Lyon 1Lyon, France; Institut des Agents Infectieux, Hospices Civils de LyonLyon, France.

Frontiers in Microbiology
|May 6, 2016
PubMed
Summary
This summary is machine-generated.

Staphylococcal enterotoxin O (SElO) uniquely halts human cell cycle progression without causing cell death. This toxin delays cells in the G0/G1 phase, potentially aiding bacterial invasion strategies.

Keywords:
G0/G1 phase delayStaphylococcus aureuscell cycle alterationcullin-3cyclomodulinenterotoxin O

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Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • The epithelial barrier is crucial for defense against pathogens like Staphylococcus aureus.
  • Staphylococcus aureus produces exotoxins that can alter host tissues.
  • Understanding exotoxin effects on host cells is vital for infection control.

Purpose of the Study:

  • To investigate the cytopathic effects of staphylococcal exotoxins SEA, SEG, SEI, SElM, SElN, and SElO on human cell lines.
  • To determine the specific impact of SElO on cell proliferation and cell cycle.
  • To identify the molecular mechanism behind SElO's effect on host cells.

Main Methods:

  • Exposure of human cell lines to various staphylococcal exotoxins.
  • Assays for cell proliferation, lactate dehydrogenase (LDH) release, and DNA fragmentation.
  • Cell cycle analysis using flow cytometry after serum starvation.
  • Yeast-two-hybrid analysis to identify SElO interacting partners.

Main Results:

  • Only staphylococcal enterotoxin O (SElO) inhibited proliferation across multiple human tumor cell lines in vitro.
  • SElO did not induce necrosis or apoptosis, as evidenced by normal LDH release and DNA fragmentation levels.
  • SElO exposure resulted in a G0/G1 cell cycle delay in synchronized human tumor cells.
  • Yeast-two-hybrid analysis identified cullin-3 as a potential binding partner for SElO, a protein involved in cell cycle regulation.

Conclusions:

  • Staphylococcal enterotoxin O (SElO) inhibits cell proliferation by delaying host cell entry into the G0/G1 phase of the cell cycle, without inducing cell death.
  • This unique cell cycle modulation by SElO may represent a strategy for S. aureus to gain an advantage during infection by arresting target cells.
  • Further research into SElO-cullin-3 interactions could reveal novel therapeutic targets for staphylococcal infections.