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Nicotine-Free e-Cigarette Vapor Exposure Stimulates IL6 and Mucin Production in Human Primary Small Airway Epithelial Cells

Authors Gellatly S, Pavelka N, Crue T, Schweitzer KS, Day BJ, Min E, Numata M, Voelker DR, Scruggs A, Petrache I, Chu HW

Received 1 January 2020

Accepted for publication 19 March 2020

Published 16 April 2020 Volume 2020:13 Pages 175—185


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Ning Quan

Shaan Gellatly, Nicole Pavelka, Taylor Crue, Kelly S Schweitzer, Brian J Day, Elysia Min, Mari Numata, Dennis R Voelker, April Scruggs, Irina Petrache, Hong Wei Chu

Department of Medicine, National Jewish Health, Denver, CO 80206, USA

Correspondence: Hong Wei Chu; Irina Petrache Tel +1 303-398-1689
; +1 303-398-2080
Fax +1 303-270-2319
; +1 303-270-1780

Purpose: Electronic cigarettes (e-cigs) are relatively new devices that allow the user to inhale a heated and aerosolized solution. At present, little is known about their health effects in the human lung, particularly in the small airways (< 2 mm in diameter), a key site of airway obstruction and destruction in chronic obstructive pulmonary disease and other acute and chronic lung conditions. The aim of this study was to investigate the effect of e-cigarettes on human distal airway inflammation and remodeling.
Methods: We isolated primary small airway epithelial cells from donor lungs without known lung disease. Small airway epithelial cells were cultured at air–liquid interface and exposed to 15 puffs vapor obtained by heating a commercially available e-cigarette solution (e-vapor) with or without nicotine. After 24 hrs of e-vapor exposure, basolateral and apical media as well as cell lysates were collected to measure the pleiotropic cytokine interleukin 6 (IL6) and MUC5AC, one of the major components in mucus.
Results: Unlike the nicotine-containing e-vapor, nicotine-free e-vapor significantly increased the amount of IL6, which was coupled with increased levels of intracellular MUC5AC protein. Importantly, a neutralizing IL6 antibody (vs an IgG isotype control) significantly inhibited the production of MUC5AC induced by nicotine-free e-vapor.
Conclusion: Our results suggest that human small airway epithelial cells exposed to nicotine-free e-vapor increase the inflammatory response and mucin production, which may contribute to distal lung airflow limitation and airway obstruction.

Keywords: electronic cigarette, small airway epithelial cells, inflammation, interleukin 6, mucus

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