Role of streptococcus gordonii surface proteins SspA/SspB and hsa in platelet function
Role of streptococcus gordonii surface proteins SspA/SspB and hsa in platelet function
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DOI：
10.1128/iai.00909-07
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发表时间：
2007-12-01
影响因子：
3.1
通讯作者：
Cox, Dermot
中科院分区：
文献类型：
--
作者：
Kerrigan, Steven W.;Jakubovics, Nicholas S.;Cox, Dermot
gordonii链球菌在感染性心内膜炎中受损心脏表面的定植取决于特定细菌表面蛋白对宿主受体的识别。然而，尽管多次尝试确定参与这种相互作用的机制，但所需细菌蛋白质的性质仍然知之甚少。本研究提供了明确的证据，表明几种gordonii表面蛋白参与与血小板的相互作用，支持血小板粘附并诱导血小板聚集。发现戈氏沙门氏菌支持强（d01 - challis、SK12、SK184和Blackburn）或中等（UB1545 Ahsa和CH1-Challis）粘附或不支持血小板粘附（M5、M99和Channon）。此外，在流动条件下，血小板在低剪切（50 s(-1)）下滚动并粘附在固定的s . gordonii上，以依赖于hsa的方式，但在剪切速率为bbb50 s（-1）时不与s . gordonii DL1相互作用。gordonii菌株诱导（d01 - challis, SK12, SK184， UB1545 Ahsa和M99）或未能诱导（M5, CH1-Challis， Channon和Blackburn）血小板聚集。利用蛋白质组学方法鉴定聚集菌株（DL1）和非聚集菌株（Blackburn）细胞壁蛋白表达差异，我们鉴定出抗原I/抗原H家族蛋白SspA和SspB。在血小板无反应性乳酸乳球菌中，SspA或SspB的过表达诱导GPIIb/ gpiia依赖性血小板聚集，类似于S. gordonii DL1，但它们不能支持血小板粘附。因此，金刺草具有独特的支持血小板粘附和诱导血小板聚集的机制。不同菌株之间的蛋白表达差异可能对感染性心内膜炎等侵袭性疾病的发病机制有重要意义。
Streptococcus gordonii colonization of damaged heart surfaces in infective endocarditis is dependent upon the recognition of host receptors by specific bacterial surface proteins. However, despite several attempts to identify the mechanisms involved in this interaction, the nature of the bacterial proteins required remains poorly understood. This study provides clear evidence that several S. gordonii surface proteins participate in the interaction with platelets to support platelet adhesion and induce platelet aggregation. S. gordonii strains were found to support strong (DL1-Challis, SK12, SK184, and Blackburn) or moderate (UB1545 Ahsa and CH1-Challis) adhesion or failed to support platelet adhesion (M5, M99, and Channon). In addition, under flow conditions, platelets rolled and subsequently adhered to immobilized S. gordonii at low shear (50 s(-1)) in an Hsa-dependent manner but did not interact with S. gordonii DL1 at any shear rate of > 50 s(-1). S. gordonii strains either induced (DL1-Challis, SK12, SK184, UB1545 Ahsa, and M99) or failed to induce (M5, CH1-Challis, Channon, and Blackburn) platelet aggregation. Using a proteomic approach to identify differential cell wall protein expression between aggregating (DL1) and nonaggregating (Blackburn) strains, we identified antigen I/antigen H family proteins SspA and SspB. The overexpression of SspA or SspB in platelet-nonreactive Lactococcus lactis induced GPIIb/GPIIIa-dependent platelet aggregation similar to that seen with S. gordonii DL1 However, they failed to support platelet adhesion. Thus, S. gordonii has distinct mechanisms for supporting platelet adhesion and inducing platelet aggregation. Differential protein expression between strains may be important for the pathogenesis of invasive diseases such as infective endocarditis.