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RESEARCH PRODUCT

A Study of the Effect of Proinflammatory Cytokines on the Epithelial Cells of Smokers, With or Without COPD

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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 IL8, IL13, and TNF 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 were determined. Results: COPD patients had significantly higher values of IL8 than healthy smokers (41 [22] pM vs 21 [12] pM). The values of IL8 correlated significantly with the severity of the obstruction (r=0.6; P<.05), dyspnea (r=0.45; P<.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.