A Study of the Effect of Proinflammatory Cytokines on the Epithelial Cells of Smokers,With or Without COPD |
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| Authors: | Alfredo De Diego Damiá Julio Cortijo Gimeno M. José Selma Ferrer Montserral León Fabregas Patricia Almudever Folch Javier Milara Paya |
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| Affiliation: | 1. Hospital Universitari i Politècnic La Fe, Valencia, Spain;2. Fundación de Investigación, Consorcio Hospital General Universitario, Valencia, Spain;3. CIBERES, Instituto de Salud Carlos III, Valencia, Spain;4. Departamento de Farmacología, Facultad de Medicina Universidad de Valencia, Spain;1. St Michael''s Hospital, Toronto, ON, Canada;2. University of Toronto, Toronto, ON, Canada;3. Toronto Western Hospital, University Health Network, Toronto, ON, Canada;1. UMRS 1269 INSERM/Sorbonne University, Nutriomics, Faculté de médecine Pitié-Salpêtrière, F-75013, Paris, France;2. Université Côte d’Azur, CNRS, Inserm, iBV, Nice, France;3. Centre National de la Recherche Scientifique, Université de Strasbourg, Institut des Neurosciences Cellulaires et Intégratives, F-67000, Strasbourg, France;4. Member of the scientific council of the Groupe d’Etude et de Recherche en Lipidomique (GERLI), France;1. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal;2. ICVS/3B''s, PT Government Associate Laboratory, Braga/Guimarães, Portugal;3. Respiratory Department, H. Sª Oliveira, Guimarães, Portugal;4. Minho Family Health Unit, Braga, Portugal;5. Department of Pneumology, Centro Hospitalar de S. João, Porto, Portugal;6. Faculty of Medicine (FMUP), University of Porto, Portugal;7. Horizonte Family Health Unit, Matosinhos, Portugal;1. A.I. Virtanen Institute, University of Eastern Finland, 70211 Kuopio, Finland |
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| Abstract: | ![]()
IntroductionCigarette 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 methodsTwenty-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 TNFα 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 TNFα were determined.ResultsCOPD 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 TNFα.ConclusionsThere 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. |
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