IFN-γregulates inflammatory responses and also may attenuate the fibrotic process. The production of TGF-βs by bronchial epithelial cells and lung mesenchymal cells may be important in modulating both airway inflammation and remodeling. Therefore, we hypothesized that IFN-γmay regulate TGF-β production in different types of airway cells. METHODS: Human bronchial epithelial cells (HBECs), the BEAS- 2B immortalized bronchial epithelial cell line, human fetal lung fibroblasts (HFL-1) and human airway smooth muscle cells (ASMC) were incubated for 24 h with various concentrations of IFN-γ in the absence or presence of TGF-β1, β2 or β3. Post-culture media were assayed for TGF-βs. The mRNA expression of TGFβ1, β2, Smad 2, 3, 4 and 7 were evaluated by quantitative real time RT-PCR. Cellular localization of Smads 2, 3, 4, and 7, Statlαp91 and Statl p84/p91 were evalu- ated by immunostaining. RESULTS: Exogenous TGF-βs significantly enhanced the release of TGF-β2 by HBECs and BEAS-2B cells and the re IFN-γregulates inflammatory responses and also may attenuate the fibrotic process. The production of TGF-βs by bronchial epithelial cells and lung mesenchymal cells may be important in modulating both airway inflammation and remodeling. Thus, we hypothesized that IFN-γmay regulate TGF-β METHODS: Human bronchial epithelial cells (HBECs), the BEAS-2B immortalized bronchial epithelial cell line, human fetal lung fibroblasts (HFL-1) and human airway smooth muscle cells (ASMC) were incubated for 24 h with various concentrations of IFN-γ in the absence or presence of TGF-β1, β2 or β3. Post-culture media were assayed for TGF-βs. The mRNA expression of TGFβ1, β2, Smad 2, 3, 4 and 7 were evaluated by quantitative real time RT-PCR. Cellular localization of Smads 2, 3, 4, and 7, Statlαp91 and Statl p84 / p91 were evaluated- ated by immunostaining. RESULTS: Exogenous TGF-βs significantly enhanced the release of TGF- HBECs and BEAS-2 B cells and the re