ADHESION OF STAPHYLOCOCCUS-AUREUS TO SURFACE-BOUND PLATELETS - ROLE OF FIBRINOGEN FIBRIN AND PLATELET INTEGRINS
ADHESION OF STAPHYLOCOCCUS-AUREUS TO SURFACE-BOUND PLATELETS - ROLE OF FIBRINOGEN FIBRIN AND PLATELET INTEGRINS
复制标题
DOI：
10.1093/infdis/167.2.312
复制
发表时间：
1993-02-01
影响因子：
6.4
通讯作者：
PROCTOR, RA
中科院分区：
文献类型：
--
作者：
HERRMANN, M;LAI, QJ;PROCTOR, RA
然而，血小板附着在人工或生物表面上与导管感染或心内膜炎的发病机制有关。参与金黄色葡萄球菌与黏附的血小板相互作用的配体仍然不完全清楚。将放射性标记的金黄色葡萄球菌Cowan 1与贴在聚甲基丙烯酸甲酯(PMMA)盖玻片上的纯化血小板孵育并洗涤。并测定粘附性。与白蛋白-PMMA的粘附性相比，血小板促进金黄色葡萄球菌的粘附性约30倍。在血浆(1%VOL/VOL)和血小板同时存在的情况下，粘附性得到广泛促进，30%(接种)的金黄色葡萄球菌粘附率(150倍)增加。用抗GPIIb/IIIa单抗或血小板活化抑制剂预处理血小板可减少血浆增强的黏附，提示血小板活化在金黄色葡萄球菌黏附中起作用。血浆增强型黏附对凝血酶拮抗剂、酶抑制剂、肝素或抗纤维蛋白原抗体敏感，提示纤维蛋白原/纤维蛋白是连接黏附的血小板和金黄色葡萄球菌所必需的。总之，金黄色葡萄球菌与固定的血小板的黏附可能在侵袭性血流感染或心内膜炎的发病机制中起作用。
Platelets adhering to artificial or biologic surfaces have been implicated in the pathogenesis of catheter infections or endocarditis; however. the ligands involved in Staphylococcus aureus interaction with adherent platelets remain incompletely understood. Radiolabeled S. aureus Cowan 1 were incubated with purified platelets adherent to polymethylmethacrylate (PMMA) coverslips and washed. and adhesion was determined. Platelets promoted adhesion of S. aureus approximately 30-fold compared with adhesion to albumin-PMMA. In the presence of both plasma (1% vol/vol) and platelets, adhesion was extensively promoted, with 30% (of inoculated) S. aureus adherent (150-fold increase). Platelet pretreatment with anti-GPIIb/IIIa monoclonal antibodies or inhibitors of platelet activation decreased plasma-enhanced adhesion, suggesting a role of platelet activation in S. aureus adhesion. Plasma-enhanced adhesion was sensitive to thrombin antagonists, proteinase inhibitors, heparin, or antifibrinogen antibodies, indicating that fibrinogen/fibrin is necessary for bridging between adherent platelets and S. aureus. In conclusion, S. aureus adhesion to immobilized platelets may play a role in the pathogenesis of invasive bloodstream infections or endocarditis.