Dissecting influenza virus pathogenesis uncovers a novel chemical approach to combat the infection.
Dissecting influenza virus pathogenesis uncovers a novel chemical approach to combat the infection.
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DOI：
10.1016/j.virol.2012.09.039
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发表时间：
2013-01-05
期刊：
影响因子：
3.7
通讯作者：
Rosen H
中科院分区：
文献类型：
--
作者：
Oldstone MB;Teijaro JR;Walsh KB;Rosen H
细胞因子风暴是一种侵略性的免疫反应，其特征在于炎症性白细胞的募集和感染部位细胞因子和趋化因子水平的夸大。在这里，我们审查的证据表明，细胞因子风暴直接导致流感病毒感染的发病率和死亡率，鞘氨醇-1-磷酸（S1 P）受体激动剂可以中止细胞因子风暴提供显着的保护，对致病性人流感病毒感染。在使用小鼠模型和人类致病性2009流感病毒的实验中，单独使用S1 P1受体激动剂可将流感病毒引起的死亡减少80%以上，而抗病毒神经氨酸酶抑制剂奥司他韦提供的保护较少（50%）。S1 P1受体激动剂和奥司他韦联合治疗的最佳保护率为96%。描述了S1 P受体激动剂作用的功能机制和肺内皮细胞在流感感染期间作为细胞因子风暴放大器所发挥的主导作用。
The cytokine storm is an aggressive immune response characterized by the recruitment of inflammatory leukocytes and exaggerated levels of cytokines and chemokines at the site of infection. Here we review evidence that cytokine storm directly contributes to the morbidity and mortality resulting from influenza virus infection and that sphingosine-1-phosphate (S1P) receptor agonists can abort cytokine storms providing significant protection against pathogenic human influenza viral infections. In experiments using murine models and the human pathogenic 2009 influenza viruses, S1P1 receptor agonist alone reduced deaths from influenza virus by over 80% as compared to lesser protection (50%) offered by the antiviral neuraminidase inhibitor oseltamivir. Optimal protection of 96% was achieved by combined therapy with the S1P1 receptor agonist and oseltamivir. The functional mechanism of S1P receptor agonist(s) action and the predominant role played by pulmonary endothelial cells as amplifiers of cytokine storm during influenza infection are described.
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