【Abstract】 Objective To investigate the role of miR-218-5p in chronic obstructive pulmonary disease and its mechanism. Methods BEAS 2B cells were divided into normal control (NC) group, cigarette smoke extract (CSE) group, Mir-NC+CSE group, Mir-218-5p+CSE group, Si-NC+CSE group, Si-LIN28B+CSE group, Mir-218-5p+pcDNA-NC+CSE group and Mir-218-5p+pcDNA-LIN28B+CSE group. The expression of Mir-218-5p was detected by RT-qPCR and apoptosis was detected by flow cytometry. Enzyme linked immunosorbent assay (ELISA) was used to detect the expression of IL-6 and TGF-β1. The expression levels of LIN28B and cleaved-caspase-3 were detected by Western blot. The targeting effect of Mir-218-5p on LIN28B was verified by double luciferase reporter gene assay. Results Compared with the NC group, the expression of miR-218-5p in BEAS2B cells of CSE group was reduced, while the apoptosis rate, LIN28B, Cleaved-caspase-3, IL-6 and TGF-β1 expression were significantly increased (P＜0.05). Compared with the miR-NC+CSE group, the apoptosis rate, Cleaved-caspase-3, IL-6 and TGF-β1 expression in BEAS2B cells of miR-218-5p+CSE group were significantly reduced (P＜0.05). Compared with the si-NC+CSE group, the apoptosis rate, Cleaved-caspase-3, IL-6, and TGF-β1 expression in BEAS2B cells of si-LIN28B+CSE group were significantly reduced (P＜0.05). Compared with miR-218-5p+pcDNA-NC+CSE group, the apoptosis rate, Cleaved-caspase-3, IL-6, and TGF-β1 expression in BEAS2B cells of miR-218-5p+pcDNA-LIN28B+CSE group were significantly increased (P＜0.05). Conclusion miR-218-5p could inhibit CSEinduced airway epithelial cell apoptosis and inflammatory response by targeting LIN28B. Therefore, miR-218-5p may be a potential therapeutic target for chronic obstructive pulmonary disease.