期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 187, 期 4, 页码 851-863出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2016.12.012
关键词
-
类别
资金
- University of Pittsburgh NIH Clinical and Translational Science Award [UL1RR024153, UL1TR000005]
- NTH [R01HL107380, R21A1117569, R011-1L122383, R01111079331, R01LM012087, R01LM009657, R01H-1122760]
- Parker B. Francis Foundation Fellowship
Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild-to-moderate disease phenotypes and recover within a few weeks. Influenza is known to cause persistent alveolitis in animal models; however, Little is known about the molecular pathways involved in this phenotype. We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic processes and inflammation, as well as transcriptomic and epigenetic changes at 21 to 60 days after infection. Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance of virus and resolution of morbidity. Influenza infection induced robust changes in the lung transcriptome, including a significant impact on inflammatory and extracellular matrix protein expression. Despite the robust changes in lung gene expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infection. Finally, we examined the impact of influenza on miRNA expression in the lung and found an increase in miR-155. miR-155 knockout mice recovered from influenza infection faster than controls and had decreased lung inflammation and endoplasmic reticulum stress. These data illuminate the dynamic molecular changes in the Lung in the weeks after influenza infection and characterize the repair process, identifying a novel role for miR-155.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据