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Abstract：
There is increasing recognition of the involvement of platelets in orchestrating inflammatory responses, driving the activation of neutrophils, monocytes and vascular endothelium, which, if poorly controlled, may lead to microvascular dysfunction. Importantly, hyperreactivity of platelets has been implicated in the pathogenesis of myocardial injury and the associated particularly high prevalence of acute cardiovascular events in patients with severe community-acquired pneumonia (CAP), of which Streptococcus pneumoniae (pneumococcus) is the most commonly encountered aetiologic agent. In this context, it is noteworthy that a number of studies have documented various mechanisms by which the pneumococcus may directly promote platelet aggregation and activation. The major contributors to platelet activation include several different types of pneumococcal adhesin, the pore-forming toxin, pneumolysin, and possibly pathogen-derived hydrogen peroxide, which collectively represent a major focus of the current review. This is followed by an overview of the limited experimental studies together with a larger series of clinical studies mainly focused on all-cause CAP, which have provided evidence in support of associations between alterations in circulating platelet counts, most commonly thrombocytopenia, and a poor clinical outcome. The final section of the review covers, albeit briefly, systemic biomarkers of platelet activation which may have prognostic potential.
摘要：
人们越来越认识到血小板参与协调炎症反应，驱动中性粒细胞的激活，单核细胞和血管内皮，which,如果控制不好，可能导致微血管功能障碍。重要的是,血小板的高反应性与严重社区获得性肺炎（CAP）患者心肌损伤的发病机理以及相关的急性心血管事件的发生率特别高有关。其中肺炎链球菌（肺炎球菌）是最常见的病原体。在这种情况下，值得注意的是，许多研究已经记录了肺炎球菌可能直接促进血小板聚集和活化的各种机制。血小板活化的主要贡献者包括几种不同类型的肺炎球菌粘附素，成孔毒素,肺炎球菌溶血素,和可能来自病原体的过氧化氢，它们共同代表了当前审查的主要重点。接下来是有限的实验研究的概述，以及一系列主要集中在全因CAP的临床研究。提供了支持循环血小板计数改变之间关联的证据，最常见的是血小板减少症，和不良的临床结果。审查的最后一部分包括，尽管短暂，血小板活化的系统性生物标志物可能具有预后潜力。
