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Extracellular Vesicle Tissue Factor Activity Assay
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Peptidoglycan from Staphylococcus aureus induces tissue factor expression and procoagulant activity in human

Eva Mattsson1, Heiko Herwald, Lars Björck

  • 1Department of Medical Microbiology, Lund University, Lund, Sweden. fa.mattsson@delta.telenordia.se

Infection and Immunity
|May 16, 2002
PubMed

Insights

Staphylococcus aureus infections trigger blood clotting by activating monocytes. Its cell wall component, peptidoglycan, induces tissue factor expression, promoting coagulation and severe infection pathology.

Area of Science:

  • Microbiology
  • Immunology
  • Hematology

Background:

  • Staphylococcus aureus is a major cause of human sepsis and endocarditis.
  • S. aureus infections involve blood coagulation, leading to microthrombi and organ dysfunction.
  • The bacterium forms fibrin clots (vegetations) in endocarditis.

Purpose of the Study:

  • To investigate the mechanism by which S. aureus induces procoagulant activity.
  • To determine the role of peptidoglycan and tissue factor in S. aureus-mediated coagulation.

Main Methods:

  • Incubation of human peripheral blood mononuclear cells with live/heat-killed S. aureus and purified peptidoglycan.
  • Assessment of procoagulant activity and tissue factor expression.
  • Use of antibodies to tissue factor, reverse transcription-PCR, ELISA, and flow cytometry.

Main Results:

  • Live and heat-killed S. aureus induced procoagulant activity in mononuclear cells.
  • Purified peptidoglycan induced concentration-dependent procoagulant activity.
  • Peptidoglycan-induced activity was dependent on tissue factor expression.
  • Tissue factor gene and protein expression were detected in peptidoglycan-stimulated cells.
  • Tissue factor was identified on the surface of CD14-positive monocytes.

Conclusions:

  • S. aureus peptidoglycan activates the extrinsic coagulation pathway.
  • This activation occurs via induction of tissue factor expression in monocytes.
  • This mechanism contributes to the pathogenicity of severe S. aureus infections.

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