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. 2011 Mar;13(3):216-25.
doi: 10.1016/j.micinf.2010.10.016. Epub 2010 Oct 29.

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

Shruti Daga  1 , 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
Affiliations

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

Shruti Daga et al. Microbes Infect. 2011 Mar.

Abstract

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 FcγRIIa 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 FcγRIIa 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 FcγRIIa 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 FcγRIIa platelet receptor polymorphisms do not influence S. aureus-platelet interactions in vitro or the clinical course of infective endocarditis.

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Figures

Fig. 1
Fig. 1
Association between GPIIIa PlA1/A2 genotype and platelet activation in patients with infective endocarditis. Data for the one PlA2/A2 patient are not depicted. PMA, platelet–monocyte aggregates. P values were determined using the Mann–Whitney U test.
Fig. 2
Fig. 2
Adherence of S. aureus strains to immobilized plasma proteins. Strains Newman (♦), 207 (●), or 209 (▪), were grown to exponential phase and incubated with doubling dilutions of immobilized bovine fibronectin (A), or grown to stationary phase and incubated with doubling dilutions of immobilized human fibrinogen (B). Adherence of strain Newman to wells incubated with BSA only was used to determine background levels (▴).
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