Background: Bronchial epithelial cells produce many types of chemokines and may contribute to lung inflammation by recruiting inflammatory cells. The CC chemokine eotaxin is a potent, eosinophil-specific chemoattractant that has been detected in the bronchial epithelium of patients with asthma. Objectives: The aim of this study was to investigate the regulatory mechanisms of chemokine production from bronchial epithelium by inflammatory cytokines, especially TH2- and TH1-derived cytokines, in bronchial asthma. Methods: BEAS-2B human bronchial epithelial cells were cultured with TNF-α, IL-4, IL-13, and IFN-γ alone or in combination, after which supernatants were assayed for eotaxin, IL-8, and RANTES proteins with ELISA. Reverse transcription–PCR was also performed. Results: TNF-α induced production of eotaxin, IL-8, and RANTES in a concentration-dependent manner. Both IL-4 and IL-13 synergistically enhanced TNF-α–induced eotaxin production, whereas IL-8 production induced by TNF-α was significantly down-regulated by the TH2-derived cytokines. IFN-γ, a TH1 cytokine, counteracted the enhancing effects of IL-4 and IL-13 on eotaxin production. RANTES production by TNF-α was not affected by IL-4 and IL-13 but was markedly enhanced by IFN-γ. Conclusions: These results suggest that TH2 cytokines are involved in preferential recruitment of eosinophils in bronchial asthma by enhancing eotaxin and reducing IL-8 production from bronchial epithelial cells and that TH1 cytokines counteract the effects of TH2 cytokines by reducing eotaxin production. (J Allergy Clin Immunol 2000;105:126-33.)