A study of the Effect of Proinflammatory Cytokines on the Epithelial Cells of Smokers, with or without COPD

Introduction: Cigarette smoke is the main cause of inflammation in COPD. The mechanisms that differentiate smokers who develop COPD are diverse. In this study, we analyzed the presence of cytokines in the respiratory secretions of smokers with or without COPD and the secretory properties of the differentiated bronchial epithelium obtained from the individuals themselves after exposure to tobacco smoke. Material and methods: Twenty-seven smokers were studied, 12 of whom had COPD that had not been previously treated with steroids. In 11, samples were obtained by means of induced sputum, and the remaining samples were collected from bronchial aspiration after bronchoscopy. Concentrations of IL-8. IL-13 and TNF alpha in the supernatant were determined. The results obtained were compared between individuals with and without COPD, and we studied their relationship with the severity of COPD as expressed by the degree of obstruction, dyspnea, presence of hypersecretion and intensity of smoking. Bronchial epithelial cell cultures were obtained by air-liquid interface in 4 smokers. The samples were exposed to increasing concentrations of cigarette smoke (5-20%) and the epithelial mRNA expressions of MUC5AC, IL8 and TNF alpha were determined. Results: COPD patients had significantly higher values of IL-8 than healthy smokers (41[22] vs. 21[12] pM). The values of IL-8 correlated significantly with the severity of the obstruction (r = 0.6; p < 0.05), dyspnea (r = 0.45; p < 0.05) and the presence of hypersecretion. There was no relationship between cytokines and the intensity or duration of the tobacco habit. Cigarette smoke produced a dose-dependent increase in the expression of RNAm for Muc5AC, IL8 and TNF alpha. Conclusions: There are differences in cytokine production (fundamentally IL8) between smokers and smokers with COPD which could be explained by the direct action of cigarette smoke on epithelial cells (C) 2011 SEPAR. Published by Elsevier Espana, S.L. All rights reserved.