Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis

Shruti Daga, James G Shepherd, J Garreth S Callaghan, Rachel K Y Hung, Dana K Dawson, Gareth J Padfield, Shi Y Hey, Robyn A Cartwright, David E Newby, J Ross Fitzgerald

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


Cardiac vegetations result from bacterium-platelet adherence, activation and aggregation, and are associated with increased morbidity and mortality in infective endocarditis. The GPIIb/IIIa and Fc¿RIIa platelet receptors play a central role in platelet adhesion, activation and aggregation induced by endocarditis pathogens such as Staphylococcus aureus, but the influence of known polymorphisms of these receptors on the pathogenesis of infective endocarditis is unknown. We determined the GPIIIa platelet antigen Pl(A1/A2) and Fc¿RIIa H131R genotype of healthy volunteers (n = 160) and patients with infective endocarditis (n = 40), and investigated the influence of these polymorphisms on clinical outcome in infective endocarditis and S. aureus-platelet interactions in vitro. Platelet receptor genotype did not correlate with development of infective endocarditis, vegetation characteristics on echocardiogram or the composite clinical end-point of embolism, heart failure, need for surgery or mortality (P > 0.05 for all), even though patients with the GPIIIa Pl(A1/A1) genotype had increased in vivo platelet activation (P = 0.001). Furthermore, neither GPIIIa Pl(A1/A2) nor Fc¿RIIa H131R genotype influenced S. aureus-induced platelet adhesion, activation or aggregation in vitro (P > 0.05). Taken together, our data suggest that the GPIIIa and Fc¿RIIa platelet receptor polymorphisms do not influence S. aureus-platelet interactions in vitro or the clinical course of infective endocarditis.
Original languageEnglish
Pages (from-to)216-225
Number of pages10
JournalMicrobes and Infection
Issue number3
Early online date29 Oct 2010
Publication statusPublished - Mar 2011


  • adult
  • aged
  • blood platelets
  • endocarditis
  • female
  • host-pathogen interactions
  • humans
  • integrin beta3
  • male
  • Middle Aged
  • platelet activation
  • polymorphism, genetic
  • receptors, IgG
  • staphylococcal infections
  • Staphylococcus aureus
  • statistics, nonparametric


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