Increased expression of microRNA-155-5p by alveolar type II cells contributes to development of lethal ARDS in H1N1 influenza A virus-infected mice.
Increased expression of microRNA-155-5p by alveolar type II cells contributes to development of lethal ARDS in H1N1 influenza A virus-infected mice.
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DOI：
10.1016/j.virol.2020.03.005
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发表时间：
2020-06
期刊：
影响因子：
3.7
通讯作者：
P. S. Woods;L. Doolittle;L. Rosas;S. P. Nana-Sinkam;Esmerina Tili;I. Davis
中科院分区：
文献类型：
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作者：
P. S. Woods;L. Doolittle;L. Rosas;S. P. Nana-Sinkam;Esmerina Tili;I. Davis
Alveolar type II (ATII) cells are essential to lung function and a primary site of influenza A virus (IAV) replication. Effects of IAV infection on ATII cell microRNA (miR) expression have not been comprehensively investigated. Infection of C57BL/6 mice with 10,000 or 100 pfu/mouse of IAV A/WSN/33 (H1N1) significantly altered expression of 73 out of 1908 mature murine miRs in ATII cells at 2 days post-infection (d.p.i.) and 253 miRs at 6 d.p.i.miR-155-5p(miR-155) showed the greatest increase in expression within ATII cells at both timepoints and the magnitude of this increase correlated with inoculum size and pulmonary edema severity. Influenza-induced lung injury was attenuated in C57BL/6-congenicmiR-155-knockout mice without affecting viral replication. Attenuation of lung injury was dependent on deletion ofmiR-155from stromal cells and was recapitulated in ATII cell-specificmiR-155-knockout mice. These data suggest that ATII cellmiR-155is a potential therapeutic target for IAV-induced ARDS.
