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Influenza lung injury: mechanisms and therapeutic opportunities

机译:流感肺损伤:机制和治疗机会

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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.
机译:在这种观点中,我们讨论了流感感染后急性肺损伤发病机制的最新发展,重点是有前途的治疗引线。 在小鼠中量化了对肺泡毛细管屏障的损伤,已经确定了试剂,其可以有助于保持阻隔完整性,例如血管素,血管素样4中和和鞘氨醇1-磷酸模拟物。 尽管其他类型的肺损伤有前途的数据,但使用间充质干细胞的研究结果令人失望。 体外,脂肪酸结合蛋白5,前列腺素E2和IFN-Gamma和Stat1之间的相互作用的作用。 最后,我们讨论了自噬在炎症细胞因子生产和病毒生命周期中的作用以及介入的疾病生命周期以及这提供干预的机会。

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