Acute respiratory distress syndrome (ARDS) is characterized by a rapid-onset respiratory failure with a mortality rate of approximately 40%. This physiologic inflammatory process is mediated by disruption of the alveolar-vascular interface, leading to pulmonary oedema and impaired oxygen exchange, which often warrants mechanical ventilation to increase survival in the acute setting. One of the least understood aspects of ARDS is the role of the platelets in this process. Platelets, which protect vascular integrity, play a pivotal role in the progression and resolution of ARDS. The recent substantiation of the age-old theory that megakaryocytes are found in the lungs has rejuvenated interest in and raised new questions about the importance of platelets for pulmonary function. In addition to primary haemostasis, platelets provide a myriad of inflammatory functions that are poised to aid the innate immune system. This review focuses on the evidence for regulatory roles of platelets in pulmonary inflammation, with an emphasis on two receptors, CLEC-2 and TLT-1. Studies of these receptors identify novel pathways through which platelets may regulate vascular integrity and inflammation in the lungs, thereby influencing the development of ARDS.

中文翻译：

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快速衰竭的肺的血小板生物学。

急性呼吸窘迫综合征（ARDS）的特征是快速发作的呼吸衰竭，死亡率约为40％。这种生理性炎症过程是由肺泡-血管界面的破坏所介导的，从而导致肺水肿和氧气交换受损，这通常需要机械通气以增加急性情况下的存活率。ARDS最少被理解的方面之一是血小板在此过程中的作用。保护血管完整性的血小板在ARDS的进展和消退中起关键作用。最近在肺中发现巨核细胞的古老理论得到证实，这引起了人们的兴趣，并提出了关于血小板对肺功能的重要性的新问题。除了主要的止血，血小板具有无数的炎症功能，可以帮助先天免疫系统。这篇综述集中在血小板在肺部炎症中的调节作用的证据上，着重于两种受体，CLEC-2和TLT-1。这些受体的研究确定了新的途径，血小板可以通过这些途径调节肺部的血管完整性和炎症，从而影响ARDS的发展。