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On-Chip Endothelial Inflammatory Phenotyping
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Staphylococcal strains vary greatly in their ability to induce an inflammatory response in endothelial cells

Matthias Grundmeier1, Lorena Tuchscherr, Michaela Brück

  • 1Institute of Medical Microbiology, University Hospital of Münster, Domagkstrasse 10, D-48149 Münster, Germany.

The Journal of Infectious Diseases
|February 6, 2010
PubMed
Abstract

Insights

Staphylococcus aureus strains lacking the accessory gene regulator (agr) quorum-sensing system are less inflammatory. This agr deficiency may allow bacteria to hide within endothelial cells, potentially causing chronic, relapsing infections.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Staphylococcus aureus is a significant pathogen causing severe endovascular infections.
  • These infections often become chronic and relapse despite antimicrobial treatment due to complex tissue interactions.

Purpose of the Study:

  • To investigate endothelial cell responses to various Staphylococcus aureus strains.
  • To understand the role of the accessory gene regulator (agr) quorum-sensing system in S. aureus virulence and host response.

Main Methods:

  • Microarray analysis was employed to study endothelial cell gene expression.
  • Different S. aureus strains were tested, including highly virulent isolates, an agr-defective strain (Cowan I), and clinical isolates.

Main Results:

  • All S. aureus strains demonstrated similar invasiveness into endothelial cells.
  • Wild-type strains significantly upregulated genes involved in innate immunity, while the agr-defective strain induced minimal changes.
  • The agr system's virulence factors, like alpha-toxin, were crucial for this inflammatory response.

Conclusions:

  • Staphylococcus aureus strains with defective agr systems induce less inflammation.
  • Agr deficiency may be a bacterial strategy for intracellular survival, evading immune detection.
  • This mechanism could contribute to the development of chronic and relapsing endovascular infections.

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