The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses
A Higham, D Bostock, G Booth… - International journal of …, 2018 - Taylor & Francis
A Higham, D Bostock, G Booth, JV Dungwa, D Singh
International journal of chronic obstructive pulmonary disease, 2018•Taylor & FrancisBackground 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, CXC motif ligand 8
(CXCL8), and lactate dehydrogenase release were measured. We also examined the effect …
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, CXC motif ligand 8
(CXCL8), and lactate dehydrogenase release were measured. We also examined the effect …
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.
Taylor & Francis Online