Staphylococcus aureus Adhesion via Spa, ClfA, and SdrCDE to Immobilized Platelets Demonstrates Shear-Dependent Behavior
Staphylococcus aureus Adhesion via Spa, ClfA, and SdrCDE to Immobilized Platelets Demonstrates Shear-Dependent Behavior
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DOI：
10.1161/01.atv.0000237606.90253.94
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发表时间：
2006-10
期刊：
影响因子：
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通讯作者：
Niraj Procopio Evagrio George;Q. Wei;P. Shin;K. Konstantopoulos;J. Ross
中科院分区：
文献类型：
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作者：
Niraj Procopio Evagrio George;Q. Wei;P. Shin;K. Konstantopoulos;J. Ross
本研究的目的是描述负责金黄色葡萄球菌-血小板粘附的分子机制作为生理相关的壁剪切应力的函数。方法和结果-使用平行板流动室对野生型、Spa−、ClfA−和SdrCDE−菌株与固定化血小板层的粘附进行定量。在没有等离子体的情况下，粘附力随着壁面剪切速率从100秒-1增加到5000秒-1而增加。血浆的存在显著增强了所有剪切水平下的粘附。外源性纤维蛋白原的添加产生的粘附水平类似于血浆在较低的剪切制度，但在较高的剪切速率增强粘附的效果递减。或者，随着剪切速率的增加，血管性血友病因子（VWF）在介导结合中起着越来越重要的作用。结论：在所有检测的切变率下，血浆蛋白的加入增强了金黄色葡萄球菌-血小板的相互作用。而纤维蛋白原在所有的剪切机制中起着重要的作用，随着壁剪切速率的增加，VWF的介导变得越来越重要。纤维蛋白原结合依赖于细菌粘附素ClfA和SdrCDE，而Spa是VWF的主要受体。
Objective—The objective of this study is to delineate the molecular mechanisms responsible for Staphylococcus aureus–platelet adhesion as a function of physiologically relevant wall shear stresses. Methods and Results—A parallel plate flow chamber was used to quantify adhesion of wild-type, Spa−, ClfA− and SdrCDE− strains to immobilized platelet layers. In the absence of plasma, adhesion increases with increasing wall shear rate from 100 to 5000 seconds−1. The presence of plasma significantly enhances adhesion at all shear levels. Addition of exogenous fibrinogen yields adhesion levels similar to plasma in the lower shear regimes, but has a diminishing effect on potentiating adhesion at higher shear rates. Alternatively, as shear rate increases von Willebrand factor (VWF) plays an increasingly significant role in mediating binding. Conclusions—Addition of plasma proteins potentiates S aureus–platelet interactions at all shear rates examined. Whereas fibrinogen plays a significant role in all shear regimes, VWF mediation becomes increasingly important as wall shear rate increases. Fibrinogen binding is dependent on bacterial adhesins ClfA and SdrCDE whereas Spa is the dominant receptor for VWF.