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

Andrew Higham, Declan Bostock, George Booth, Josiah V. Dungwa, Dave Singh

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)989-1000
Number of pages12
JournalInternational Journal of COPD
Volume13
Early online date23 Mar 2018
DOIs
Publication statusPublished - 2018

Keywords

  • Air–liquid interface
  • Cigarette smoke
  • COPD
  • E-cigs
  • Epithelial cells

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