Electronic cigarette liquid increases inflammation and virus infection in primary human airway epithelial cells.

Qun Wu,Di Jiang,Maisha Minor,Hong Wei Chu,Samithamby Jeyaseelan

doi:10.1371/journal.pone.0108342

Qun Wu, Di Jiang + Show 3 more

Open Access

https://doi.org/10.1371/journal.pone.0108342

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Journal: PloS one	Publication Date: Sep 22, 2014
Citations: 201	License type: CC BY 4.0

Affiliation: National Jewish Health, University of Colorado Denver

Abstract

Background/ObjectiveThe use of electronic cigarettes (e-cigarettes) is rapidly increasing in the United States, especially among young people since e-cigarettes have been perceived as a safer alternative to conventional tobacco cigarettes. However, the scientific evidence regarding the human health effects of e-cigarettes on the lung is extremely limited. The major goal of our current study is to determine if e-cigarette use alters human young subject airway epithelial functions such as inflammatory response and innate immune defense against respiratory viral (i.e., human rhinovirus, HRV) infection.Methodology/Main ResultsWe examined the effects of e-cigarette liquid (e-liquid) on pro-inflammatory cytokine (e.g., IL-6) production, HRV infection and host defense molecules (e.g., short palate, lung, and nasal epithelium clone 1, SPLUNC1) in primary human airway epithelial cells from young healthy non-smokers. Additionally, we examined the role of SPLUNC1 in lung defense against HRV infection using a SPLUNC1 knockout mouse model. We found that nicotine-free e-liquid promoted IL-6 production and HRV infection. Addition of nicotine into e-liquid further amplified the effects of nicotine-free e-liquid. Moreover, SPLUNC1 deficiency in mice significantly increased lung HRV loads. E-liquid inhibited SPLUNC1 expression in primary human airway epithelial cells. These findings strongly suggest the deleterious health effects of e-cigarettes in the airways of young people. Our data will guide future studies to evaluate the impact of e-cigarettes on lung health in human populations, and help inform the public about potential health risks of e-cigarettes.

Highlights

Electronic cigarettes (e-cigarettes) are battery-operated devices that heat up e-cigarette liquid (e-liquid) without or with nicotine and turn it into an inhalable vapor
Our data suggest that even nicotine-free e-liquid promotes pro-inflammatory response and Human rhinovirus (HRV) infection
Both eliquid without nicotine and with nicotine inhibits lung innate immunity (e.g., SPLUNC1) that is involved in lung defense against HRV infection

Summary

Introduction

Electronic cigarettes (e-cigarettes) are battery-operated devices that heat up e-cigarette liquid (e-liquid) without or with nicotine and turn it into an inhalable vapor. Perceived as a safer alternative to conventional tobacco cigarettes, the use of e-cigarettes has increased rapidly in the United States (U.S.). Despite banning ecigarette sales to minors in some U.S states, e-cigarettes can be purchased in bordering states or via the Internet [1]. A notable proportion of adolescents and young adults who had never smoked tobacco cigarettes have used e-cigarettes. About 1.78 million U.S youth had ever used e-cigarettes as of 2012 [2]. While e-cigarette manufacturers claim that their products are harmless, adverse respiratory effects (e.g., cough, wheezing and pneumonia) have been reported in social media from e-cigarette users [3]. The scientific evidence regarding the human health effects of e-cigarettes on the lung is extremely limited

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