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Related Experiment Videos

Staphylococcal alpha-toxin causes increased tracheal epithelial permeability.

James R Phillips1, Timothy J Tripp, Warren E Regelmann

  • 1Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota 55455, USA. phill071@umn.edu

Pediatric Pulmonology
|September 26, 2006
PubMed
Summary

Staphylococcus aureus alpha-toxin damages airway epithelium, increasing permeability and causing cell detachment. This study clarifies the toxin's role in pulmonary infections by demonstrating direct epithelial injury.

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Area of Science:

  • Pulmonary Medicine
  • Microbiology
  • Toxicology

Background:

  • Staphylococcus aureus is a significant cause of lung infections.
  • The specific role of S. aureus alpha-toxin in virulence is not fully understood.
  • Airway epithelium is a potential target for S. aureus toxins.

Purpose of the Study:

  • To investigate if S. aureus alpha-toxin independently damages airway epithelium.
  • To measure the effects of alpha-toxin on tracheal epithelial permeability and structure.
  • To test the hypothesis that airway epithelium is a direct target of S. aureus alpha-toxin.

Main Methods:

  • Development of an isolated whole mouse trachea test apparatus.
  • Measurement of in vitro epithelial permeability (P).

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  • Morphometric analysis of digital micrographs to assess epithelial adhesion.

    • Main Results:

    • Purified S. aureus alpha-toxin significantly increased tracheal epithelial permeability (P < 0.05).
    • Morphometric analysis showed a dose-dependent decrease in epithelial adhesion to the basement membrane with alpha-toxin exposure (P < 0.05).
    • The novel trachea model demonstrated increased permeability and epithelial-basement membrane separation upon alpha-toxin exposure.

    Conclusions:

    • Mammalian airway epithelium is a direct target of Staphylococcus aureus alpha-toxin.
    • S. aureus alpha-toxin contributes to airway damage during pulmonary infections.
    • The developed trachea model is effective for studying toxin-induced epithelial damage.