Cigarette smoke differently alters normal and ovalbumin-sensitized bronchial epithelial cells from rat

Smoking is a common habit in the general population, even in asthmatic patients. Bronchial epithelial cells are the first cellular elements exposed to environmental stimuli such as cigarette smoke. These cells produce a wide range of mediators involved in inflammation and remodeling processes. However, the effects of chronic smoke exposure on the release and production of these mediators remain unclear.

To investigate the effects of repeated exposure to cigarette smoke extract on mediator released by bronchial epithelial cells isolated from control and asthmatic rats.

Bronchial epithelial cells were isolated from normal (NRBE) and asthmatic rats (ARBE) (ovalbumin (OVA)-sensitized rat). Cells were exposed to cigarette smoke extract (CSE) obtained by impacting cigarette smoke with an AGI-30. A concentration of 3% CSE was added in the medium daily, for 5 consecutive days. Supernatant was recovered at baseline and after the 5 days. Levels of macrophage chemoattractant protein (MCP)-1, interleukin (IL)-10, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF), IL-1alpha, and interferon (IFN)-gamma were measured using enzyme-linked immunosorbent assay (ELISA).

TNF, IL-1alpha, and IFN-gamma were lower than the detection limit of our methods. At the baseline, NRBE produced less MCP-1 but more IL-10 and VEGF when compared with ARBE. CSE exposure reduced NRBE IL-10 production but did not significantly alter MCP-1 and VEGF production. Interestingly, bronchial epithelial cells of asthmatic rats responded differently to CSE. MCP-1 level was decreased and VEGF increased after CSE exposure, whereas IL-10 level did not change in ARBE.

Cells isolated from asthmatic rats produced distinct levels of mediators compared with cells isolated from control rats. Furthermore, these cells react differently to CSE exposure.