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首页> 外文期刊>Infection and immunity >Staphylococcus aureus susceptibility to thrombin-induced platelet microbicidal protein is independent of platelet adherence and aggregation in vitro.
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Staphylococcus aureus susceptibility to thrombin-induced platelet microbicidal protein is independent of platelet adherence and aggregation in vitro.

机译：金黄色葡萄球菌对凝血酶诱导的血小板杀微生物蛋白的敏感性与体外血小板粘附和聚集无关。

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Bacterium-platelet interactions at the cardiac valve surface represent an important initial step in the induction of infective endocarditis (IE). This cell-cell interaction may play either a protagonistic role in the induction of IE via bacterial adherence to and aggregation of platelets or an antagonistic role via secretion of platelet-derived microbicidal molecules. We examined the spectrum and interrelationship of three aspects of the interaction of 20 clinical Staphylococcus aureus isolates with rabbit platelets in vitro: (i) S. aureus adherence to platelets; (ii) S. aureus-induced platelet aggregation; and (iii) S. aureus resistance to the action of thrombin-induced platelet microbicidal protein (PMP; low-molecular-weight cationic peptides contained in alpha granules). Among the 20 S. aureus isolates (11 bacteremia, 9 endocarditis), there was a heterogeneous distribution profile for each of the bacterium-platelet interaction parameters studied. For S. aureus-platelet adherence and S. aureus-induced platelet aggregation, 3 of 20 and 7 of 20 isolates tested were considered highly active for each respective parameter; 5 of 20 staphylococcal strains were deemed resistant to the bactericidal action of PMP. In addition, more endocarditis isolates (45%) were PMP resistant than strains from patients without endocarditis (19%). When analyzed concomitantly, there was a significant, positive correlation between S. aureus-platelet adherence and S. aureus-induced platelet aggregation among isolates (P = 0.003; r = 0.78). In contrast, there were no statistically significant relationships between either platelet adherence or aggregation and PMP resistance among these 20 S. aureus isolates. These data suggest that platelet adherence and aggregation are related abilities of S. aureus, while resistance to thrombin-induced PMP is an independent phenotypic characteristic and potential virulence factor.
机译：心脏瓣膜表面的细菌-血小板相互作用代表了感染性心内膜炎（IE）诱导中重要的初始步骤。这种细胞间的相互作用可能通过细菌对血小板的粘附和聚集而在IE的诱导中起主要作用，或者通过血小板衍生的杀微生物分子的分泌而发挥拮抗作用。我们研究了20种临床金黄色葡萄球菌分离物与兔血小板相互作用的三个方面的光谱和相互关系：（i）金黄色葡萄球菌对血小板的粘附; （ii）金黄色葡萄球菌诱导的血小板聚集; （iii）金黄色葡萄球菌对凝血酶诱导的血小板杀微生物蛋白（PMP;α颗粒中所含的低分子量阳离子肽）的抗性。在20种金黄色葡萄球菌分离株中（11种菌血症，9种心内膜炎），每种细菌-血小板相互作用参数均存在异质分布。对于金黄色葡萄球菌-血小板粘附和金黄色葡萄球菌诱导的血小板凝集，被测试的20个菌株中的3个和20个菌株中的7个被认为对每个参数均具有高活性。 20个葡萄球菌菌株中有5个被认为对PMP的杀菌作用具有抗性。此外，与无心内膜炎患者的菌株相比，分离出的心内膜炎菌株（45％）对PMP有抵抗力（19％）。同时进行分析时，分离株之间金黄色葡萄球菌-血小板粘附和金黄色葡萄球菌诱导的血小板聚集之间存在显着正相关（P = 0.003; r = 0.78）。相反，在这20个金黄色葡萄球菌分离株中，血小板粘附或聚集与PMP抗性之间没有统计学上的显着关系。这些数据表明血小板粘附和聚集是金黄色葡萄球菌的相关能力，而对凝血酶诱导的PMP的抗性是独立的表型特征和潜在的毒力因子。

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