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首页> 外文期刊>American Journal of Physiology >Characteristics of new Staphylococcus aureus-RBC adhesion mechanism independent of fibrinogen and IgG under hydrodynamic shear conditions.
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Characteristics of new Staphylococcus aureus-RBC adhesion mechanism independent of fibrinogen and IgG under hydrodynamic shear conditions.

机译：在流体动力剪切条件下，新的金黄色葡萄球菌-RBC粘附机制的特征独立于纤维蛋白原和IgG。

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Staphylococcus aureus infection begins when bacterial cells circulating in blood adhere to components of the extracellular matrix or endothelial cells of the host and initiate colonization. S. aureus is known to exhibit extensive interactions with platelets. S. aureus is also known to bind to red blood cells (RBCs) in the presence of plasma proteins, such as fibrinogen and IgG. Herein we report a new binding mechanism of S. aureus to RBC independent of those plasma proteins. To characterize the new adhesion mechanism, we experimentally examine the binding kinetics and molecular constituents mediating the new adhesive interactions between S. aureus and RBCs under defined shear conditions. The results demonstrate that the receptors for fibrinogen (clumping factor A) and IgG (protein A) of S. aureus are not involved in the adhesion. S. aureus binds to RBCs with maximal adhesion at the shear rate 100 s(-1) and decreasing adhesion with increasing shear. The heteroaggregates formed after shear are stable when subjected to the shear rate 2,000 s(-1), indicating that intercellular contact time rather than shear forces controls the adhesion at high shear. S. aureus binding to RBC requires plasma, and 10% plasma is sufficient for maximal adhesion. Plasma proteins involved in the cell-cell adhesion, such as fibrinogen, fibronectin, von Willebrand factor, IgG, thrombospondin, laminin, and vitronectin are not involved in the observed adhesion. The extent of heteroaggregation is dramatically reduced on RBC treatment with trypsin, chymotrypsin, or neuraminidase, suggesting that the receptor(s) mediating the heteroaggregation process is a sialylated glycoprotein on RBC surface. Adhesion is divalent cation dependent and also blocked by heparin. This work demonstrates a new mechanism of S. aureus-RBC binding under hydrodynamic shear conditions via unknown RBC sialoglycoprotein(s). The binding requires plasma protein(s) other than fibrinogen or IgG and does not involve the S. aureus adhesins clumping factor A or protein A.
机译：当血液中循环的细菌细胞粘附于宿主细胞外基质或内皮细胞的成分并开始定植时，金黄色葡萄球菌感染就开始了。已知金黄色葡萄球菌表现出与血小板的广泛相互作用。还已知在血浆蛋白（例如纤维蛋白原和IgG）存在下，金黄色葡萄球菌会与红细胞（RBC）结合。在本文中，我们报告了金黄色葡萄球菌与RBC的新结合机制，独立于那些血浆蛋白。为了表征新的粘附机制，我们在规定的剪切条件下，通过实验研究了介导金黄色葡萄球菌和RBC之间新的粘附相互作用的结合动力学和分子成分。结果表明，金黄色葡萄球菌的纤维蛋白原（聚集因子A）和IgG（蛋白A）的受体不参与粘附。金黄色葡萄球菌在剪切速率为100 s（-1）时以最大粘附力与RBC结合，并随着剪切力的增加而降低粘附力。剪切后形成的杂聚集体在受到2,000 s（-1）的剪切速率时是稳定的，表明细胞间的接触时间而不是剪切力控制着高剪切力下的粘附。金黄色葡萄球菌与RBC的结合需要血浆，而10％的血浆足以获得最大的粘附力。参与细胞粘附的血浆蛋白，例如纤维蛋白原，纤连蛋白，血管性血友病因子，IgG，血小板反应蛋白，层粘连蛋白和玻连蛋白不参与观察到的粘附。在用胰蛋白酶，胰凝乳蛋白酶或神经氨酸酶进行RBC处理时，杂聚的程度显着降低，表明介导杂聚过程的受体是RBC表面的唾液酸化糖蛋白。粘附是二价阳离子依赖性的，并且也被肝素阻断。这项工作证明了通过未知的RBC唾液糖蛋白在水动力剪切条件下金黄色葡萄球菌RBC结合的新机制。结合需要血纤蛋白原或IgG以外的血浆蛋白，并且不涉及金黄色葡萄球菌粘附素聚集因子A或蛋白A。

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