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

• Published in: Microbes and infection Vol. 13; no. 3; pp. 216 - 225
• Main Authors: Daga, Shruti, Shepherd, James G., Callaghan, J. Garreth S., Hung, Rachel K.Y., Dawson, Dana K., Padfield, Gareth J., Hey, Shi Y., Cartwright, Robyn A., Newby, David E., Fitzgerald, J. Ross
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Masson SAS 01.03.2011; Elsevier
• Subjects: Adult; Aged; Bacteriology; Biological and medical sciences; Blood Platelets - microbiology; Blood Platelets - physiology; Endocarditis; Endocarditis - blood; Endocarditis - genetics; Endocarditis - microbiology; Female; Fundamental and applied biological sciences. Psychology; Genetic polymorphisms; Host-Pathogen Interactions; Humans; Integrin beta3 - genetics; Male; Microbiology; Middle Aged; Miscellaneous; Original; Platelet Activation; Platelet aggregation; Polymorphism, Genetic; Receptors, IgG - genetics; Staphylococcal Infections - blood; Staphylococcal Infections - genetics; Staphylococcal Infections - microbiology; Staphylococcus aureus; Staphylococcus aureus - physiology; Statistics, Nonparametric; Platelet aggregation; Genetic polymorphisms; Endocarditis; Cardiovascular disease; Aggregation; Platelet; Heart disease; Endocardial disease; Bacteria; Micrococcales; Genetics; Micrococcaceae; Staphylococcus aureus; Polymorphism

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...