BACKGROUND: There have been a few reports suggesting involvement of neutrophil as well as eosinophil in inducing bronchoconstriction aft,er inhalation of TDI. OBJECTIVE: In order to observe the source of chemokines in TDI-induced asthma, this investigation was designed to determine whether IL-8 and RANTES could be produced by human bronchial epithelial cells and whether dexamethasone had any effects on their production. Materials and METHODS: We cultured Beas-2B, a bronchial epithelial cell line, with five concentrations of TDI-human serum albumin (HSA) conjugate and compared them with those having no conjugate. The levels of IL-8 and RANTES in the supernatant were measured by ELISA. To evaluate the effect of pro-inflammatory cytokines, cells were incubated with peripheral blood mononuclear cell (PBMC) culture supernatant, which was derived from PBMC culture of a TDI -induced asthmatic subject under exposure to TDI-HSA conjugate, and then compared to those without PBMC supernatant addition. To evaluate the effect of dexamethasone, four concentrations of dexamethasone were pre-incubated and the same steps were repeated. RESULTS: There was significant production of IL-8 from bronchial epithelial cells with addition of TDI-HSA conjugate in a dose-dependent manner (p<0.05, respectively), which was significantly augmented with additions of PBMC supernatant (p<0.05, respectively) at each concentration. RANTES production was negligible, however, it increased significantly with addition of PBMC supernatant and TDI-HSA conjugate in a dose response manner(p<0.05, respectively). Compared to the untreated sample, pre-treatment of dexamethasone induced remarkable inhibitions of IL-8 and RANTES production. CONCLUSION: These results suggest that IL-8 and RANTES released from bronchial epithelial cells may contribute to neutrophil and eosinophil recruitment occurring in TDI-induced airway.