Endothelial activation and dysfunction in the pathogenesis of influenza A virus infection.
Endothelial activation and dysfunction in the pathogenesis of influenza A virus infection.
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DOI：
10.4161/viru.25779
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发表时间：
2013-08-15
期刊：
影响因子：
5.2
通讯作者：
Lee WL
中科院分区：
文献类型：
--
作者：
Armstrong SM;Darwish I;Lee WL
严重流感的发展被部分归因于先天免疫反应的增强。最近的证据表明，内皮细胞的激活、屏障功能的丧失以及随之而来的微血管泄漏也可能在严重流感的发病机制中发挥重要的作用。本综述的目的是总结目前支持内皮细胞激活和功能障碍是严重流感发生前的中心特征的证据。我们还讨论了流感对血小板-内皮细胞相互作用的影响。
The development of severe influenza has been attributed, in part, to a heightened innate immune response. Recent evidence suggests that endothelial activation, loss of barrier function, and consequent microvascular leak may also serve important mechanistic roles in the pathogenesis of severe influenza. The aim of this review is to summarize the current evidence in support of endothelial activation and dysfunction as a central feature preceding the development of severe influenza. We also discuss the effect of influenza on platelet–endothelial interactions.