The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses

Andrew Higham,1,2 Declan Bostock,1 George Booth,2 Josiah V Dungwa,2 Dave Singh1,2 1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and University...

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Main Authors: Higham A, Bostock D, Booth G, Dungwa JV, Singh D
Format: Article
Language:English
Published: Dove Medical Press 2018-03-01
Series:International Journal of COPD
Subjects:
Online Access:https://www.dovepress.com/the-effect-of-electronic-cigarette-and-tobacco-smoke-exposure-on-copd--peer-reviewed-article-COPD
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author Higham A
Bostock D
Booth G
Dungwa JV
Singh D
author_facet Higham A
Bostock D
Booth G
Dungwa JV
Singh D
author_sort Higham A
collection DOAJ
description Andrew Higham,1,2 Declan Bostock,1 George Booth,2 Josiah V Dungwa,2 Dave Singh1,2 1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and University Hospital of South Manchester, NHS Foundation Trust, Manchester, UK; 2Medicines Evaluation Unit, University Hospital of South Manchester, Manchester, UK Background: Electronic cigarettes (e-cigs) are used to help smoking cessation. However, these devices contain harmful chemicals, and there are safety concerns. We have investigated the effects of e-cigs on the inflammatory response and viability of COPD bronchial epithelial cells (BECs).Methods: BECs from COPD patients and controls were exposed to e-cig vapor extract (ECVE) and the levels of interleukin (IL)-6, C-X-C motif ligand 8 (CXCL8), and lactate dehydrogenase release were measured. We also examined the effect of ECVE pretreatment on polyinosinic:polycytidylic acid (poly I:C)-stimulated cytokine release from BECs. Parallel experiments using Calu-3 cells were performed. Comparisons were made with cigarette smoke extract (CSE).Results: ECVE and CSE caused an increase in the release of IL-6 and CXCL8 from Calu-3 cells. ECVE only caused toxicity in BECs and Calu-3 cells. Furthermore, ECVE and CSE dampened poly I:C-stimulated C-X-C motif ligand 10 release from both cell culture models, reaching statistical significance for CSE at an optical density of 0.3.Conclusion: ECVE caused toxicity and reduced the antiviral response to poly I:C. This raises concerns over the safety of e-cig use. Keywords: e-cigs, epithelial cells, COPD, air–liquid interface, cigarette smoke
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spelling doaj.art-ccc0d15f20c64b6880fd8fdb04ba32db2022-12-22T02:03:31ZengDove Medical PressInternational Journal of COPD1178-20052018-03-01Volume 13989100037401The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responsesHigham ABostock DBooth GDungwa JVSingh DAndrew Higham,1,2 Declan Bostock,1 George Booth,2 Josiah V Dungwa,2 Dave Singh1,2 1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and University Hospital of South Manchester, NHS Foundation Trust, Manchester, UK; 2Medicines Evaluation Unit, University Hospital of South Manchester, Manchester, UK Background: Electronic cigarettes (e-cigs) are used to help smoking cessation. However, these devices contain harmful chemicals, and there are safety concerns. We have investigated the effects of e-cigs on the inflammatory response and viability of COPD bronchial epithelial cells (BECs).Methods: BECs from COPD patients and controls were exposed to e-cig vapor extract (ECVE) and the levels of interleukin (IL)-6, C-X-C motif ligand 8 (CXCL8), and lactate dehydrogenase release were measured. We also examined the effect of ECVE pretreatment on polyinosinic:polycytidylic acid (poly I:C)-stimulated cytokine release from BECs. Parallel experiments using Calu-3 cells were performed. Comparisons were made with cigarette smoke extract (CSE).Results: ECVE and CSE caused an increase in the release of IL-6 and CXCL8 from Calu-3 cells. ECVE only caused toxicity in BECs and Calu-3 cells. Furthermore, ECVE and CSE dampened poly I:C-stimulated C-X-C motif ligand 10 release from both cell culture models, reaching statistical significance for CSE at an optical density of 0.3.Conclusion: ECVE caused toxicity and reduced the antiviral response to poly I:C. This raises concerns over the safety of e-cig use. Keywords: e-cigs, epithelial cells, COPD, air–liquid interface, cigarette smokehttps://www.dovepress.com/the-effect-of-electronic-cigarette-and-tobacco-smoke-exposure-on-copd--peer-reviewed-article-COPDe-cigsepithelial cellsCOPDair–liquid interfacecigarette smoke
spellingShingle Higham A
Bostock D
Booth G
Dungwa JV
Singh D
The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
International Journal of COPD
e-cigs
epithelial cells
COPD
air–liquid interface
cigarette smoke
title The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
title_full The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
title_fullStr The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
title_full_unstemmed The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
title_short The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
title_sort effect of electronic cigarette and tobacco smoke exposure on copd bronchial epithelial cell inflammatory responses
topic e-cigs
epithelial cells
COPD
air–liquid interface
cigarette smoke
url https://www.dovepress.com/the-effect-of-electronic-cigarette-and-tobacco-smoke-exposure-on-copd--peer-reviewed-article-COPD
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