Airway epithelial‐derived exosomes induce acute asthma exacerbation after respiratory syncytial virus infection

作者：Ye Yao, Yu Yang, Ming Ji, Qingwu Qin, Kun Xu, Zhenkun Xia, Huijun Liu, Lin Yuan, Yunchang Yuan, Ling Qin, Xizi Du, Leyuan Wang, Kai Zhou, Xinyu Wu, Weijie Wang, Bei Qing, Yang Xiang, Xiangping Qu, Ming Yang, Xiaoqun Qin, Chi Liu · 发表于：MedComm · 年份：2024 · DOI：10.1002/mco2.621 · 被引用次数：8 · 研究领域：Respiratory viral infections research、Extracellular vesicles in disease、Neonatal Respiratory Health Research

Acute asthma exacerbation refers to the progressive deterioration of asthma symptoms that is always triggered by virus infection represented by respiratory syncytial virus (RSV). After RSV infection, exaggerated Th2-mediated pulmonary inflammation is the critical pathological response of asthmatic patients with acute exacerbation. Significantly, airway epithelial cells, being the primary targets of RSV infection, play a crucial role in controlling the pulmonary inflammatory response by releasing airway epithelial cell-derived exosomes (AEC-Exos), which potentially influence the development of asthma. However, the specific role of AEC-Exos in acute asthma exacerbation after RSV infection remains obscure. The purpose of this study was to determine the distinct function of AEC-Exos in exacerbating acute asthma following RSV infection. Blockade of exosomes by GW reduce the enhanced pulmonary inflammation significantly. Specifically, the enhanced Th2 inflammation was induced by AEC-Exos thorough transportation of hsa-miR-155-5p-Sirtuin 1 (SIRT1) pathway during acute asthma exacerbation. Targeted inhibition of hsa-miR-155-5p blocks the exaggerated Th2 inflammation effectively in mice with acute asthma exacerbation. In summary, our study showed that during acute asthma exacerbation after RSV infection, AEC-Exos promote the enhanced Th2 inflammation through transportation of increased hsa-miR-155-5p, which was mediated partly through SIRT1-mediated pathway. hsa-miR-155-5p is a potent...