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 journalArticle

9 Citations (Scopus)

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 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
Volume13
Issue number3
Early online date29 Oct 2010
DOIs
Publication statusPublished - Mar 2011

Fingerprint

Endocarditis
Staphylococcus aureus
Blood Platelets
Integrin beta3
Platelet Activation
Platelet Aggregation
Genotype
varespladib methyl
Mortality
Embolism
Healthy Volunteers
Heart Failure
Morbidity
Bacteria
Antigens
In Vitro Techniques

Keywords

  • 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

Cite this

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

In: Microbes and Infection, Vol. 13, No. 3, 03.2011, p. 216-225.

Research output: Contribution to journalArticle

Daga, S, Shepherd, JG, Callaghan, JGS, Hung, RKY, Dawson, DK, Padfield, GJ, Hey, SY, Cartwright, RA, Newby, DE & Fitzgerald, JR 2011, 'Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis', Microbes and Infection, vol. 13, no. 3, pp. 216-225. https://doi.org/10.1016/j.micinf.2010.10.016
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. / Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis. In: Microbes and Infection. 2011 ; Vol. 13, No. 3. pp. 216-225.
@article{1a2954dcd5b3413897da344d18a2c845,
title = "Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis",
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 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.",
keywords = "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",
author = "Shruti Daga and Shepherd, {James G} and Callaghan, {J Garreth S} and Hung, {Rachel K Y} and Dawson, {Dana K} and Padfield, {Gareth J} and Hey, {Shi Y} and Cartwright, {Robyn A} and Newby, {David E} and Fitzgerald, {J Ross}",
note = "Copyright {\circledC} 2010 Institut Pasteur. All rights reserved.",
year = "2011",
month = "3",
doi = "10.1016/j.micinf.2010.10.016",
language = "English",
volume = "13",
pages = "216--225",
journal = "Microbes and Infection",
issn = "1286-4579",
publisher = "Elsevier Masson SAS",
number = "3",

}

TY - JOUR

T1 - Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis

AU - Daga, Shruti

AU - Shepherd, James G

AU - Callaghan, J Garreth S

AU - Hung, Rachel K Y

AU - Dawson, Dana K

AU - Padfield, Gareth J

AU - Hey, Shi Y

AU - Cartwright, Robyn A

AU - Newby, David E

AU - Fitzgerald, J Ross

N1 - Copyright © 2010 Institut Pasteur. All rights reserved.

PY - 2011/3

Y1 - 2011/3

N2 - 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.

AB - 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.

KW - adult

KW - aged

KW - blood platelets

KW - endocarditis

KW - female

KW - host-pathogen interactions

KW - humans

KW - integrin beta3

KW - male

KW - Middle Aged

KW - platelet activation

KW - polymorphism, genetic

KW - receptors, IgG

KW - staphylococcal infections

KW - Staphylococcus aureus

KW - statistics, nonparametric

U2 - 10.1016/j.micinf.2010.10.016

DO - 10.1016/j.micinf.2010.10.016

M3 - Article

VL - 13

SP - 216

EP - 225

JO - Microbes and Infection

JF - Microbes and Infection

SN - 1286-4579

IS - 3

ER -