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血小板受体多态性并不影响金黄色葡萄球菌与血小板的相互作用或感染性心内膜炎。

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

机构信息

Center for Infectious Diseases and The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Chancellor's Building, Edinburgh EH164SB, United Kingdom.

出版信息

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

DOI:10.1016/j.micinf.2010.10.016
PMID:21044892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3036801/
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.

摘要

心瓣膜赘生物是由细菌-血小板黏附、激活和聚集引起的，与感染性心内膜炎的发病率和死亡率增加有关。血小板受体 GPIIb/IIIa 和 FcγRIIa 在金黄色葡萄球菌等感染性心内膜炎病原体引起的血小板黏附、激活和聚集中起核心作用，但这些受体的已知多态性对感染性心内膜炎发病机制的影响尚不清楚。我们确定了健康志愿者（n=160）和感染性心内膜炎患者（n=40）的血小板抗原 GPIIIa Pl(A1/A2)和 FcγRIIa H131R 基因型，并研究了这些多态性对感染性心内膜炎临床结局和金黄色葡萄球菌-血小板相互作用的影响。血小板受体基因型与感染性心内膜炎的发生、超声心动图上的赘生物特征或栓塞、心力衰竭、需要手术或死亡的复合临床终点均无相关性（所有 P 值均>0.05），尽管 GPIIIa Pl(A1/A1)基因型患者体内血小板激活增加（P=0.001）。此外，GPIIIa Pl(A1/A2)和 FcγRIIa H131R 基因型均不影响金黄色葡萄球菌诱导的血小板黏附、激活或聚集（P>0.05）。总之，我们的数据表明，GPIIIa 和 FcγRIIa 血小板受体多态性不影响体外金黄色葡萄球菌-血小板相互作用或感染性心内膜炎的临床病程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cf3/3036801/63435a78b030/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cf3/3036801/16624e52b805/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cf3/3036801/63435a78b030/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cf3/3036801/16624e52b805/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cf3/3036801/63435a78b030/gr2.jpg

相似文献

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引用本文的文献

[1]
A comparison of different antibiotic regimens for the treatment of infective endocarditis.

Cochrane Database Syst Rev. 2020-5-14

[2]
Inherited Variation in Cytokine, Acute Phase Response, and Calcium Metabolism Genes Affects Susceptibility to Infective Endocarditis.

Mediators Inflamm. 2017

[3]
Genetic variants in genes of the inflammatory response in association with infective endocarditis.

PLoS One. 2014-10-9

[4]
Platelets: at the nexus of antimicrobial defence.

Nat Rev Microbiol. 2014-6

[5]
A novel core genome-encoded superantigen contributes to lethality of community-associated MRSA necrotizing pneumonia.

PLoS Pathog. 2011-10-13

本文引用的文献

[1]
Genetic variation in Fc gamma receptor IIa and risk of coronary heart disease: negative results from two large independent populations.

BMC Med Genet. 2009-5-29

[2]
Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study.

Arch Intern Med. 2009-3-9

[3]
Long-term outcome of infective endocarditis: a study on patients surviving over one year after the initial episode treated in a Finnish teaching hospital during 25 years.

BMC Infect Dis. 2008-4-17

[4]
Technetium 99m-labeled annexin V scintigraphy of platelet activation in vegetations of experimental endocarditis.

Circulation. 2008-2-12

[5]
Alpha and beta chains of hemoglobin inhibit production of Staphylococcus aureus exotoxins.

Biochemistry. 2007-12-18

[6]
Direct vascular effects of protease-activated receptor type 1 agonism in vivo in humans.

Circulation. 2006-10-10

[7]
Hemostasis and aging.

Crit Rev Oncol Hematol. 2006-11

[8]
The interaction of bacterial pathogens with platelets.

Nat Rev Microbiol. 2006-6

[9]
Molecular mechanisms of prothrombotic risk due to genetic variations in platelet genes: Enhanced outside-in signaling through the Pro33 variant of integrin beta3.

Exp Biol Med (Maywood). 2006-5

[10]
Update on infective endocarditis.

Curr Probl Cardiol. 2006-4

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