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Elucidating the role of Staphylococcus epidermidis serine-aspartate repeat protein G in platelet activation

M P Brennan1, A Loughman, M Devocelle

  • 1Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland.

Journal of Thrombosis and Haemostasis : JTH
|June 3, 2009
PubMed
Abstract

Insights

Staphylococcus epidermidis serine-aspartate repeat protein G (SdrG) directly causes platelet aggregation and adhesion. This interaction involves fibrinogen and IgG, highlighting SdrG

Area of Science:

  • Microbiology
  • Hematology
  • Biochemistry

Background:

  • Staphylococcus epidermidis is a skin commensal linked to medical device infections.
  • S. epidermidis induces platelet aggregation via an unknown mechanism.
  • The fibrinogen-binding protein SdrG is prevalent in clinical strains.

Purpose of the Study:

  • To investigate the role of SdrG in platelet activation.
  • To elucidate the mechanism of SdrG-mediated platelet aggregation, focusing on fibrinogen's role.

Main Methods:

  • Expressed SdrG in Lactococcus lactis to isolate its function.
  • Utilized platelet adhesion and aggregation assays.
  • Employed alpha(IIb)beta3 antagonists, aspirin, and Bbeta-chain fibrinopeptide for inhibition studies.

Main Results:

  • L. lactis expressing SdrG induced significant platelet aggregation.
  • Aggregation was dependent on fibrinogen, IgG, and the FcgammaRIIa receptor.
  • SdrG directly mediated platelet adhesion via alpha(IIb)beta3 and indirectly via fibrinogen/IgG bridges.

Conclusions:

  • SdrG alone can initiate platelet adhesion and aggregation.
  • Both direct and indirect mechanisms contribute to SdrG's pro-thrombotic effects.
  • SdrG is a key virulence factor in S. epidermidis-associated infections.

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