Cigarette smoke is associated with a high morbidity and mortality, and affects particularly the respiratory tract. Various in vitro models have been developed to study the effects of cigarette smoke on bronchial epithelial cells. To identify an adequate exposure model of cigarette smoke, we analysed the effects of cigarette smoke extract (CSE) and a smoking chamber on bronchial epithelial cells. The release of monocyte chemoattractant protein (MCP)-1, interleukin (IL)-10, and vascular endothelial growth factor (VEGF) was measured. Bronchial epithelial cells isolated from Sprague-Dawley rat (NRBE) were exposed to 3% CSE or air control every day for 3 days. In the second model, NRBE were placed in an air/liquid interface and exposed, in a smoking chamber, to whole smoke from 2 cigarettes, twice daily for 3 days. Levels of MCP-1, IL-10, and VEGF were measured by enzyme-linked immunosorbent assay (ELISA), 24 h after the last exposure. The pattern of MCP-1 production by bronchial epithelial cells was different between the two models. MCP-1 release was increased after 3 days of exposure in the CSE model, but was inhibited using the smoking chamber model. Production of IL-10 by NRBE was reduced after 3 days in both models. Finally, no difference was observed in the production of VEGF between the two models. CSE and the smoking chamber differently modulate bronchial epithelial cell mediator production, demonstrating that the model of cigarette smoke exposure used can influence the data obtained.