Objective To investigate the effects of cigarette smoke extract (CSE)-induced macrophage conditioned medium on the inflammatory response of airway epithelial cells, and explore the underlying mechanisms. Methods Monocyte/macrophages (THP-1) were differentiated by PMA (20 ng/mL) for 24 hours,and then treated with 10% CSE for 24 hours, and their conditioned medium was collected to induce inflammatory responses human bronchial epithelial cells (BEAS-2B). The effects of THP-1 cell conditioned medium on BEAS-2B cell viability were detected by the CCK-8 assay. The mRNA expression of inflammatory cytokines in BEAS-2B cell were analyzed by quantitative PCR. The secretion of inflammatory cytokines were measured by ELISA. The effect of conditioned medium on the morphology of BEAS-2B cells was observed by immunofluorescence staining .The proteins expression related to mTORC1/p70S6K pathway were examined bySWB. Results The viability BEAS-2B cells treated with 6.25%, 12.5%, or 25% conditioned medium showed no significant changes at the time course of 6, 12, 24, or 48 h. The conditioned medium with the concentration of 50%, 75%, and 100% induced significant reductions in cell viability (p<0.05, p<0.01). The mRNA expression levels of IL-1β, IL-6, IL-8, and TNF-α in BEAS-2B cells were significantly upregulated (p<0.05, p<0.01), and the levels of IL-1β, IL-6, and IL-8 in supernatants were significantly increased in all concentration groups (p<0.05, p<0.01). Furthermore, in conditioned medium-treated cells, the levels of p-mTOR, p-p70S6K, and p-GSK3β (Tyr216) were significantly increased (p<0.05, p<0.01), However, there was little effect on cell morphology. Conclusion The conditioned medium of CSE-stimulated macrophages significantly induces inflammatory responses in airway epithelial cells by activating the mTORC1/p70S6K pathway.