Differences between Cytokine Release from Bronchial Epithelial Cells of Asthmatic Patients and Non–Asthmatic Subjects: Effect of Exposure to Diesel Exhaust Particles

Abstract

Background: Recent evidence suggests that the airways of asthmatics are more susceptible to adverse effects of air pollutants than the airways of non–asthmatics, but the underlying mechanisms are not clear. Methods: We have cultured bronchial epithelial cells (HBEC) from biopsies of atopic mild asthmatic patients and non–atopic non–asthmatic subjects, and investigated constitutive and diesel exhaust particles (DEP)–induced release of several pro–inflammatory mediators. Results: HBEC of asthmatic patients constitutively released significantly greater amounts of IL–8, GM–CSF and sICAM–1 than HBEC of non–asthmatic subjects. RANTES was only released by HBEC of asthmatic patients. Incubation of the asthmatic cultures with 10 μg/ml DEP significantly increased the release of IL–8, GM–CSF and sICAM–1 after 24 h. In contrast, only the higher concentrations of 50–100 μg/ml DEP significantly increased the release of IL–8 and GM–CSF from HBEC of non–asthmatics. Conclusions: These results suggest that the increased sensitivity of the airways of asthmatics to air pollutants such as DEP may, at least in part, be a consequence of greater constitutive and pollutant–induced release of specific pro–inflammatory mediators from their bronchial epithelial cells.