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Direct interaction of iron-regulated surface determinant IsdB of Staphylococcus aureus with the GPIIb/IIIa receptor

Helen Miajlovic1, Marta Zapotoczna1, Joan A Geoghegan1

  • 1Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College Dublin, Dublin 2, Ireland.

Microbiology (Reading, England)
|December 17, 2009
PubMed

Insights

Staphylococcus aureus uses iron-regulated surface determinant B (IsdB) to directly bind platelets, causing aggregation and potentially endovascular infections. This interaction is crucial for bacterial pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Bacterial interaction with platelets contributes to endovascular infections, with Staphylococcus aureus being a primary cause.
  • S. aureus surface proteins typically mediate platelet aggregation via fibrinogen/fibronectin, requiring antibodies.

Purpose of the Study:

  • To investigate S. aureus's interaction with platelets under iron-limited conditions, mimicking in vivo environments.
  • To identify novel bacterial factors involved in platelet adhesion and aggregation.

Main Methods:

  • Culturing S. aureus in iron-limited medium.
  • Utilizing S. aureus mutants lacking specific surface proteins.
  • Employing antibodies and antagonists targeting platelet integrin GPIIb/IIIa.
  • Surface plasmon resonance to assess direct protein interactions.

Main Results:

  • Under iron limitation, an S. aureus mutant lacking known platelet-activating proteins adhered directly to platelets, inducing aggregation without plasma proteins.
  • Inhibition of iron-regulated surface determinant (Isd) proteins prevented platelet adhesion and aggregation.
  • A specific Isd protein, IsdB, was identified as essential for platelet adhesion and aggregation; mutants lacking IsdB showed no interaction.
  • Antibodies and antagonists targeting platelet integrin GPIIb/IIIa blocked adhesion mediated by IsdB-expressing S. aureus.
  • Recombinant IsdB directly binds to platelet integrin GPIIb/IIIa.

Conclusions:

  • Iron-regulated surface determinant B (IsdB) is a key S. aureus surface protein mediating direct platelet adhesion and aggregation.
  • IsdB interaction with platelet integrin GPIIb/IIIa is a novel mechanism contributing to S. aureus pathogenesis in endovascular infections.
  • Targeting the IsdB-GPIIb/IIIa interaction could offer therapeutic strategies against S. aureus infections.

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