Aberrant coagulation causes a hyper-inflammatory response in severe influenza pneumonia.
Aberrant coagulation causes a hyper-inflammatory response in severe influenza pneumonia.
复制标题
异常凝血导致严重流感肺炎的高炎症反应
DOI：
10.1038/cmi.2016.1
复制
发表时间：
2016-07
影响因子：
24.1
通讯作者：
Tang H
中科院分区：
文献类型：
--
作者：
Yang Y;Tang H
甲型流感病毒（IAV）感染人类的呼吸道，每年在全世界引起显著的发病率和死亡率。侵袭性炎症，被称为细胞因子风暴，被认为是IAV感染期间肺部大部分损伤的原因。功能性凝血障碍是致病性流感常见的并发症，表现为肺内皮细胞活化、血管渗漏、弥散性血管内凝血和肺微栓塞。重要的是，新出现的证据表明，不受控制的凝血系统，包括细胞（内皮细胞和血小板）和蛋白质（凝血因子，抗凝剂和纤维蛋白溶解蛋白酶）成分，有助于通过增强病毒复制和免疫发病机制的流感的发病机制。本文就凝血功能障碍在IAV发病机制中的作用机制作一综述。
Influenza A virus (IAV) infects the respiratory tract in humans and causes significant morbidity and mortality worldwide each year. Aggressive inflammation, known as a cytokine storm, is thought to cause most of the damage in the lungs during IAV infection. Dysfunctional coagulation is a common complication in pathogenic influenza, manifested by lung endothelial activation, vascular leak, disseminated intravascular coagulation and pulmonary microembolism. Importantly, emerging evidence shows that an uncontrolled coagulation system, including both the cellular (endothelial cells and platelets) and protein (coagulation factors, anticoagulants and fibrinolysis proteases) components, contributes to the pathogenesis of influenza by augmenting viral replication and immune pathogenesis. In this review, we focus on the underlying mechanisms of the dysfunctional coagulatory response in the pathogenesis of IAV.