Title |
The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
|
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Published in |
International Journal of Chronic Obstructive Pulmonary Disease, March 2018
|
DOI | 10.2147/copd.s157728 |
Pubmed ID | |
Authors |
Andrew Higham, Declan Bostock, George Booth, Josiah V Dungwa, Dave Singh |
Abstract |
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). 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). 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. ECVE caused toxicity and reduced the antiviral response to poly I:C. This raises concerns over the safety of e-cig use. |
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Demographic breakdown
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Scientists | 4 | 13% |
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Mendeley readers
Geographical breakdown
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Demographic breakdown
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Researcher | 21 | 13% |
Student > Master | 13 | 8% |
Student > Ph. D. Student | 12 | 8% |
Other | 7 | 4% |
Other | 16 | 10% |
Unknown | 60 | 38% |
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Other | 31 | 19% |
Unknown | 67 | 42% |