B族链球菌不同菌株对血小板的活化作用

 目的: 探索B族链球菌(GBS)不同菌株对血小板活化的作用及可能的机制。方法: 来自脓毒症伴血小板减少患者分离鉴定的6株GBS作为诱导剂,分别采用血小板聚集仪、流式细胞术、扫描电镜和Western blotting方法检测它们对血小板聚集率以及血小板膜蛋白CD62P、TLR2和TLR4表达的影响;进一步用TLR2和TLR4单克隆抗体封闭血小板表面TLR2和TLR4以检测它们与GBS诱导的血小板活化的关系。结果: 6株GBS中有3株可诱导血小板聚集,且能明显上调血小板TLR2和CD62P的表达(P < 0.05),但对血小板TLR4的表达没有影响;封闭血小板TLR2后,GBS诱导的血小板聚集率明显下降。结论: 部分GBS菌株可诱导血小板活化,血小板TLR2可能在这个过程中起重要作用。

Effects of different group B streptococci strains on platelet activation

AIM: To explore the ability of different group B streptococci (GBS) strains on inducing platelet activation. METHODS: Six strains of GBS, separated from the septic patients with thrombocytopenia, were used as the inducers. Light transmission aggregometry was used to measure platelet aggregation. Scanning electron microscopy (SEM) was performed to investigate the interaction of platelets with bacteria. The expression of platelet CD62P, Toll-like receptor 2 (TLR2) and TLR4 was determined by flow cytometry and Western blotting. Furthermore, the activity of platelet TLR2 (or TLR4) was blocked by anti-TLR2 (or anti-TLR4) monoclonal antibody, and the platelet aggregation induced by GBS was detected. RESULTS: Only 3 of 6 GBS strains isolated from the septic patients induced platelet aggregation and up-regulated the expression of CD62P and TLR2 in the platelets (P < 0.05), but not TLR4. Incubation with anti-TLR2 antibody, but not anti-TLR4 antibody, significantly blocked platelet aggregation induced by GBS.CONCLUSION: Some GBS strains from the patients are able to trigger platelet activation in vitro, and platelet TLR2 may play an important role in the interaction between GBS and platelets.