Objective:To investigate the mechanism of overexpression of miR-320e in inhibiting inflammatory response of re-spiratory syncytial virus(RSV)infected bronchial epithelial cells.Methods:Human bronchial epithelial cells 16HBE were cultured in vitro and infected with RSV,and cells were divided into Con group,RSV group,RSV+miR-NC group,RSV+miR-320e group,RSV+miR-320e+vector group,RSV+miR-320e+TLR4 group.RT-qPCR was used to detect expression levels of miR-320e and TLR4 mRNA;MTT to detect cell proliferation changes;flow cytometry to detect cell apoptosis;Western blot was used to detect Bcl-2,Bax,TLR4,IκBα,p-IκBα,NF-κB and p-NF-κB protein expressions;ELISA to detect TNF-α,IL-6,IL-1β and IFN-α,IFN-β expres-sions;dual luciferase experiment to verify the tageting relationship between miR-320e and TLR4.Results:Compared with Con group,miR-320e expression level,survival rate,Bcl-2 and IκBα protein expressions were significantly reduced,apoptosis rate,Bax protein expression,TNF-α,IL-6,IL-1β and IFN-α,IFN-β expressions,TLR4 mRNA and protein expression,and p-IκBα protein expres-sion and p-NF-κB/NF-κB were increased significantly in RSV group.Compared with RSV+miR-NC group,miR-320e expression level,survival rate,IFN-α,IFN-β expressions,Bcl-2 and IκBα protein expressions were significantly increased,apoptosis rate,Bax pro-tein expression,TNF-α,IL-6,IL-1β expressions,TLR4 mRNA and protein expression,and p-IκBα protein expression and p-NF-κB/NF-κB in RSV+miR-320e group were significantly reduced.miR-320e targets and negatively regulates the expression of TLR4.Up-regulation of TLR4 can partially restore the effect of overexpression of miR-320e on apoptosis and inflammatory response of RSV-infected bronchial epithelial cells 16HBE.Conclusion:miR-320e inhibits 16HBE apoptosis and inflammation in RSV-infected bronchial epi-thelial cells by targeting and negatively regulating TLR4 expression.