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临床分离的粪肠球菌可聚集人血小板。

Clinical isolates of Enterococcus faecalis aggregate human platelets.

机构信息

Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.

出版信息

Microbes Infect. 2010 Apr;12(4):295-301. doi: 10.1016/j.micinf.2010.01.005. Epub 2010 Jan 28.

DOI:10.1016/j.micinf.2010.01.005
PMID:20109578
Abstract

Many endocarditis pathogens activate human platelets and this has been proposed to contribute to virulence. Here we report for the first time that many clinical isolates of Enterococcus faecalis, a common pathogen in infective endocarditis, aggregate human platelets. 84 isolates from human blood and urine were screened for their ability to aggregate platelets from four different donors. Platelet aggregation occurred for between 11 and 65% of isolates depending on the donor. In one donor, a significantly larger proportion of isolates from blood than from urine caused platelet aggregation. Median time to aggregation was 11 min and had a tendency to be shorter for blood isolates as compared to urine isolates. Immunoglobulin G (IgG) was shown to be essential in mediating activation and aggregation. Platelet aggregation could be abolished by an IgG-specific proteinase (IdeS), by an antibody blocking FcRgammaIIa on platelets, or by preabsorption of plasma with an E. faecalis isolate. Fibrinogen binding to bacteria or platelets does not contribute to platelet activation or aggregation under our experimental conditions. These results indicate that platelet activation and aggregation by E. faecalis is dependent on both host and bacterial factors and that it may be involved in the pathogenesis of invasive disease with this organism.

摘要

许多心内膜炎病原体能激活人类血小板,这被认为有助于其毒力。在这里,我们首次报道,许多临床分离的粪肠球菌,一种感染性心内膜炎的常见病原体,能聚集人类血小板。从人血液和尿液中筛选了 84 株分离物,以检测它们是否能聚集来自 4 个不同供体的血小板。血小板聚集的发生率在 11%至 65%之间,取决于供体。在一个供体中,血液来源的分离物比尿液来源的分离物引起血小板聚集的比例显著更高。聚集的中位时间为 11 分钟,且血液分离物的聚集时间较尿液分离物更短。免疫球蛋白 G(IgG)被证明是介导激活和聚集所必需的。血小板聚集可以被 IgG 特异性蛋白酶(IdeS)、阻断血小板 FcRgammaIIa 的抗体或用粪肠球菌分离物预吸收血浆来消除。在我们的实验条件下,纤维蛋白原与细菌或血小板的结合并不能导致血小板的激活或聚集。这些结果表明,粪肠球菌对血小板的激活和聚集依赖于宿主和细菌因素,这可能与该病原体引起的侵袭性疾病的发病机制有关。

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