〔Abstract〕 Objective To investigate the effect and mechanism of microRNA-223(miR-223) on the inflammatory response, oxidative stress and apoptosis of human bronchial epithelial cells(BEAS-2 B) induced by influenza A virus(IAV). Methods RT-qPCR was used to detect the expression of miR-223 andNLRP3 mRNA in sera of influenza patients and normal people, and the effect of IAV treatment at different time on the mRNA expression of miR-223 and NLRP3 was detected; CCK-8 was used to detect the cell viability of BEAS-2 B. Annexin V-FITC/PI apoptosis detection kit was used to detect the apoptosis level of BEAS-2 B cells. The expression of apoptosis related proteins Caspase-3, Caspase-9, Bax and Bcl-2 was detected by Western blot; ROS was detected by reactive oxygen species indicator DCFH-DA. Results The results showed that the expression of miR-223 in the serum of influenza patients was lower than that of normal people; IAV inhibited miR-223 and promoted the mRNA expression ofNLRP3, which was time-dependent(P<0.05). Overexpression of miR-223 reduced the apoptosis rate and inflammatory factor levels of BEAS-2 B induced by IAV(P<0.05). In addition, overexpression of miR-223 alleviated oxidative stress of BEAS-2 B induced by IAV(P<0.05). Further study showed that miR-223 inhibited the expression of TLR4, p-p65 and NLRP3(P<0.05). Conclusion miR-223 alleviated the oxidative stress, apoptosis and reduced cell damage of pulmonary epithelial cells induced by IAV by inhibiting TLR4/NF-κB signaling pathway and activating NLRP3 inflammasome.