Increased expression of microRNA-155-5p by alveolar type II cells contributes to development of lethal ARDS in H1N1 influenza A virus-infected mice
| Autor: | Lucia E. Rosas, Ian C. Davis, Lauren M. Doolittle, Esmerina Tili, Parker S. Woods, S. Patrick Nana-Sinkam |
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| Rok vydání: | 2020 |
| Předmět: |
ARDS
Stromal cell Cell Biology Lung injury medicine.disease_cause Article Virus Mice 03 medical and health sciences Influenza A Virus H1N1 Subtype Virology Influenza Human microRNA medicine Influenza A virus Animals Humans 030304 developmental biology Mice Knockout Respiratory Distress Syndrome 0303 health sciences 030302 biochemistry & molecular biology respiratory system medicine.disease Mice Inbred C57BL MicroRNAs medicine.anatomical_structure Viral replication Alveolar Epithelial Cells Cancer research Female |
| Zdroj: | Virology |
| ISSN: | 0042-6822 |
| Popis: | 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-congenic miR-155-knockout mice without affecting viral replication. Attenuation of lung injury was dependent on deletion of miR-155 from stromal cells and was recapitulated in ATII cell-specific miR-155-knockout mice. These data suggest that ATII cell miR-155 is a potential therapeutic target for IAV-induced ARDS. |
| Databáze: | OpenAIRE |
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