Objective This study investigated the effects of cigarette smoke extract ( CSE)-induced macrophage-conditioned medium on airway epithelial cells?? inflammatory responses, and explored the underlying mechanisms involved. Methods Phorbol myristate acetate-induced differentiated monocytes and macrophages (THP-1) were cultured with 10% CSE for 24 h; the conditioned medium was collected to induce inflammatory responses in human bronchial epithelial cells (BEAS-2B). The effects of THP-1-conditioned medium on BEAS-2B cells viability were detected using the CCK-8 assay. The effects of conditioned medium on mRNA expression levels of inflammationrelated factors in BEAS-2B cells were analyzed by RT-qPCR, and inflammatory cytokine secretion was measured with enzyme-linked immunosorbent assay. The effects of conditioned medium on BEAS-2B cells morphology were observed with immunofluorescence staining. The expression of proteins related to the mTOR/ p70S6K pathway was examined by Western blot. Results BEAS-2B cells viability after treatment with 6. 25%, 12. 5%, or 25% conditioned medium showed no significant changes after 6, 12, 24, or 48 h, while 50%, 75%, and 100% induced significant reductions in cell viability (P<0. 05, P<0. 01). Conditioned medium at 6. 25%, 12. 5%, and 25% significantly increased the mRNA expression and secretion of inflammatory factors interleukin ( IL)-1β, IL-6, IL-8, and TNF-α in BEAS-2B cells(P<0. 05, P<0. 01), but had no significant effect on morphology. Levels of p-mTOR, p-p70S6K, p-GSK3β (Tyr216), and p-NF-κB p65 were significantly increased in conditioned medium-treated cells (P<0. 05, P<0. 01);the mTORC1 inhibitor rapamycin significantly reduced inflammatory factor mRNA expression in BEAS-2B cells induced by 25% conditioned medium. Conclusions CSE-induced macrophage-conditioned medium significantly induced airway epithelial cell inflammatory responses through activating the mTORC1 / p70S6K pathway.