Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia.
Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia.
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DOI：
10.3389/fimmu.2020.577303
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发表时间：
2020
影响因子：
7.3
通讯作者：
Anderson R
中科院分区：
文献类型：
--
作者：
Feldman C;Anderson R
社区获得性肺炎（CAP）仍然是世界范围内发病率和死亡率的重要原因，最近和正在进行的研究主要集中在感染期间心血管事件（CVEs）的发生，这与不良的短期和长期生存有关。许多旨在阐明这些事件发病机制的研究都是在实验和临床CAP的背景下进行的，CAP由危险的细菌性呼吸道病原体肺炎链球菌（肺炎球菌）引起，肺炎链球菌仍然是CAP最常见的细菌性病因。这种类型的研究表明，虽然血小板在宿主防御感染中发挥重要作用，但也越来越多地认识到这些细胞的过度活化有助于促炎性、促血栓形成的全身环境，这有助于CVE的病因学。在肺炎球菌的情况下，血小板驱动的心肌损伤和功能障碍由于肺炎球菌溶血素的直接心脏毒性作用而加剧，肺炎球菌溶血素是该病原体的主要成孔毒素，其也充当血小板的有效激活剂。本文综述了血小板在宿主防御感染，特别是肺炎球菌感染中的作用，并回顾了目前的文献，描述了血小板活化导致CAP心血管并发症的潜在机制。在此之前，对CAP中肺炎球菌感染的负担、CVE的临床特征和推定的致病机制进行了评价，并对大环内酯类抗血小板活性和各种预防性治疗的潜在效用进行了评价。
Community-acquired pneumonia (CAP) remains an important cause of morbidity and mortality throughout the world with much recent and ongoing research focused on the occurrence of cardiovascular events (CVEs) during the infection, which are associated with adverse short-term and long-term survival. Much of the research directed at unraveling the pathogenesis of these events has been undertaken in the settings of experimental and clinical CAP caused by the dangerous, bacterial respiratory pathogen, Streptococcus pneumoniae (pneumococcus), which remains the most common bacterial cause of CAP. Studies of this type have revealed that although platelets play an important role in host defense against infection, there is also increasing recognition that hyperactivation of these cells contributes to a pro-inflammatory, prothrombotic systemic milieu that contributes to the etiology of CVEs. In the case of the pneumococcus, platelet-driven myocardial damage and dysfunction is exacerbated by the direct cardiotoxic actions of pneumolysin, a major pore-forming toxin of this pathogen, which also acts as potent activator of platelets. This review is focused on the role of platelets in host defense against infection, including pneumococcal infection in particular, and reviews the current literature describing the potential mechanisms by which platelet activation contributes to cardiovascular complications in CAP. This is preceded by an evaluation of the burden of pneumococcal infection in CAP, the clinical features and putative pathogenic mechanisms of the CVE, and concludes with an evaluation of the potential utility of the anti-platelet activity of macrolides and various adjunctive therapies.