Influenza lung injury: mechanisms and therapeutic opportunities
Influenza lung injury: mechanisms and therapeutic opportunities
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DOI：
10.1152/ajplung.00283.2015
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发表时间：
2015-11-15
影响因子：
4.9
通讯作者：
Kobzik, Lester
中科院分区：
文献类型：
--
作者：
Gregory, David J.;Kobzik, Lester
在这个视角中，我们讨论了流感感染后急性肺损伤发病机制的一些最新进展，重点是有希望的治疗线索。已经对小鼠肺泡-毛细血管屏障的损害进行了量化，并发现了有助于保持屏障完整性的药物，如血管生成素、血管生成素样中和和1-磷酸鞘氨醇模拟物。使用间充质干细胞的研究结果令人失望，尽管在其他类型的肺损伤方面有希望的数据。脂肪酸结合蛋白5、前列腺素E2的作用以及干扰素-γ和STAT1在感染过程中上皮信号转导中的相互作用已在体外进行了研究。最后，我们讨论了自噬在炎性细胞因子产生和病毒生命周期中的作用，以及这为干预提供的机会。
In this Perspectives, we discuss some recent developments in the pathogenesis of acute lung injury following influenza infection, with an emphasis on promising therapeutic leads. Damage to the alveolar-capillary barrier has been quantified in mice, and agents have been identified that can help to preserve barrier integrity, such as vasculotide, angiopoietin-like 4 neutralization, and sphingosine 1-phosphate mimics. Results from studies using mesenchymal stem cells have been disappointing, despite promising data in other types of lung injury. The roles of fatty acid binding protein 5, prostaglandin E2, and the interplay between IFN-gamma and STAT1 in epithelial signaling during infection have been addressed in vitro. Finally, we discuss the role of autophagy in inflammatory cytokine production and the viral life cycle and the opportunities this presents for intervention.