Abstract: Objective To investigate the role of mammalian target of rapamycin (mTOR) activation in menthol-induced expression of airway inflammation- related factors in human bronchial epithelial cells and explore its mechanism. Methods Cultured human bronchial epithelial cells (BEAS-2B) were divided into normal control group, menthol group, rapamycin group, and menthol+rapamycin group with corresponding treatments. The cell viability was measured with CCK-8 method. The mRNA levels of transient receptor potential melastatin 8 (TRPM8), tumor necrosis factor (TNF)-α and interleukin (IL)-1β were detected by RT-PCR, and the protein expressions of phosphorylated mTOR (p-mTOR), TRPM8, TNF-α and IL-1β were determined using Western blotting. The intracellular Ca2 + fluorescence intensity was measured by flow cytometry. Results Compared with the normal control cells, menthol- treated cells showed significantly increased TNF-α, IL-1β, and p-mTOR expression and elevated intracellular Ca2 + concentration (P<0.05), and the rapamycin-treated cells exhibited significantly decreased p-mTOR expression (P<0.05). No significant difference was found in TNF-α, IL-1β or intracellular Ca2+ concentration between the normal control and rapamycin-treated cells (P>0.05). Compared with the menthol-treated cells, the cells treated with both menthol and rapamycin showed significantly decreased TNF- α, IL-1β, and p-mTOR expression and obviously lowered intracellular Ca2 + concentration (P<0.05). Conclusion Menthol promotes the expressions of airway inflammationrelated factors IL-1β and TNF-α possibly by activating mTOR to cause the increase of intracellular Ca2+ concentration.