流感病毒抑制呼吸道上皮细胞中对氨氯地平敏感的钠离子通道。
Influenza virus inhibits amiloride-sensitive Na+ channels in respiratory epithelia.
作者信息
Kunzelmann K, Beesley A H, King N J, Karupiah G, Young J A, Cook D I
机构信息
Departments of Physiology and Pathology, and Medical Foundation of the University of Sydney, University of Sydney, New South Wales 2006, Australia.
出版信息
Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10282-7. doi: 10.1073/pnas.160041997.
Abstract
Many pathogens causing diarrhea do so by modulating ion transport in the gut. Respiratory pathogens are similarly associated with disturbances of fluid balance in the respiratory tract, although it is not known whether they too act by altering epithelial ion transport. Here we show that influenza virus A/PR/8/34 inhibits the amiloride-sensitive Na(+) current across mouse tracheal epithelium with a half-time of about 60 min. We further show that the inhibitory effect of the influenza virus is caused by the binding of viral hemagglutinin to a cell-surface receptor, which then activates phospholipase C and protein kinase C. Given the importance of epithelial Na(+) channels in controlling the amount of fluid in the respiratory tract, we suggest that down-regulation of Na(+) channels induced by influenza virus may play a role in the fluid transport abnormalities that are associated with influenza infections.
摘要
许多引起腹泻的病原体是通过调节肠道中的离子运输来实现的。呼吸道病原体同样与呼吸道液体平衡紊乱有关，尽管尚不清楚它们是否也通过改变上皮离子运输起作用。在此我们表明，甲型流感病毒A/PR/8/34抑制小鼠气管上皮细胞上的氨氯地平敏感钠电流，半衰期约为60分钟。我们进一步表明，流感病毒的抑制作用是由病毒血凝素与细胞表面受体结合引起的，随后激活磷脂酶C和蛋白激酶C。鉴于上皮钠通道在控制呼吸道液体量方面的重要性，我们认为流感病毒诱导的钠通道下调可能在与流感感染相关的液体运输异常中起作用。
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