Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

Christian Herr,Andreas Keller,Li Dong,Loïc Guillot,Christina Backes,Julia Niederstraßer,Konstantinos Tsitouras,Robert Bals,Christoph Beisswenger

doi:10.1186/s12931-020-1317-2

Abstract

BackgroundThe use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE).MethodsWe exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR.ResultsBacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples.ConclusionThe transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use.

Highlights

The use of electronic cigarettes (ECIGs) is increasing, but the impact of Electronic cigarette (ECIG)-vapor on cellular processes like inflammation or host defense are less understood
To determine whether ECIGs have an effect on epithelial host defense, we exposed human Calu3 cells to Traditional cigarette (TCIG) or the corresponding amount of ECIG-vapor and infected the cells with 1 × 103 Colony forming units (CFU) P. aeruginosa
Based on gene expression analysis, the expression patterns of TCIG-exposed cells were more different from sham exposed cells than ECIG-exposed cells

Summary

Introduction

The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE). ECIGs are devices that produce a vapor by heating a liquid [3] that usually contains a mixture of glycerol, propylene-glycol, water, flavors, and different concentrations of nicotine. Glycerol-propylene-glycol-water mixtures have been in use for a long time as artificial fog in aviation emergency training and entertainment business, but only a few studies about possible side effects exist before the emergence of ECIGs [5, 6].

Objectives

Methods

Results

Conclusion