Beijing Institute of Basic Medical Sciences, Beijing, P. R. China.
Platelets. 2011;22(3):228-36. doi: 10.3109/09537104.2010.543962. Epub 2011 Jan 25.
Several fibrinogen binding proteins (Fibs) play important roles in the pathogenesis of Staphylococcus aureus (S. aureus). Most Fibs can promote the aggregation of platelets during infection, but the extracellular fibrinogen-binding protein (Efb) is an exception. It is reported that Efb can specifically bind fibrinogen and inhibit the aggregation of platelet with its N terminal. However, the biological significance of platelet aggregation inhibition in the infection caused by S. aureus is unclear until now. Here, we demonstrated that the persistence and aggregation of platelets were important for killing S. aureus in whole blood. It was found that the N terminal of Efb (EfbN) and platelets inhibitors could increase the survival of S. aureus in whole blood. The study in vivo also showed that EfbN and platelets inhibitors could reduce the killing of S. aureus and increase the lethality rate of S. aureus in the acute infection mouse model.
几种纤维蛋白原结合蛋白（Fibs）在金黄色葡萄球菌（S. aureus）的发病机制中发挥着重要作用。大多数 Fibs 在感染过程中可以促进血小板聚集，但细胞外纤维蛋白原结合蛋白（Efb）是个例外。据报道，Efb 可以特异性结合纤维蛋白原，并通过其 N 端抑制血小板聚集。然而，直到现在，金黄色葡萄球菌感染中血小板聚集抑制的生物学意义尚不清楚。在这里，我们证明了血小板的持续存在和聚集对于全血中金黄色葡萄球菌的杀伤至关重要。研究发现，Efb 的 N 端（EfbN）和血小板抑制剂可以增加金黄色葡萄球菌在全血中的存活。体内研究也表明，EfbN 和血小板抑制剂可以降低金黄色葡萄球菌的杀伤作用，并增加急性感染小鼠模型中金黄色葡萄球菌的致死率。
