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Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in infants and children. The present study aimed to investigate the effects of miR-146a on RSV replication and the related mechanisms. Material and methods: We pretreated A549 and HEp-2 cells and young rats with miR-146a mimic before infection with RSV. The expressions of miR-146a and RSV-F mRNA in cells and lung tissues were detected by RT-qPCR, and production of IL-1β, IL-6, IL-18, and TNF-α in bronchial alveolar lavage fluid (BALF) were determined by ELISA. The expression level of TRAF-6 and activation of the JNK/ERK/MAPK/NF-κB signaling pathway was detected by Western blotting. Results: RSV infection significantly reduced miR-146a levels in both A549 and HEp-2 cells and rat lung tissues. RSV infection resulted in accelerated growth, increased release of inflammatory cytokines, increased expression of TRAF-6, and activation of the JNK pathway in cells, and the lung inflammatory infiltration and the pathological score increased in rats. Overexpression of miR-146a targeted down-regulation of TRAF-6 expression and JNK/ERK/MAPK/NF-κB pathway induced by RSV infection, reduced the production of inflammatory cytokines IL-1β, IL-6 and TNF-α, and alleviate lung injury in young rats. We got similar results in both A549 and HEp-2 cell experiments. Conclusion: MiR-146a alleviates lung injury caused by RSV infection in young rats by targeting TRAF-6 and regulating JNK/ERK/MAPK signaling pathways.

MiR-146a alleviates lung injury caused by RSV infection in young rats by targeting TRAF-6 and regulating JNK/ERKMAPK signaling pathways