Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

Abstract

Background: 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). Methods: We 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. Results: Bacterial 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. Conclusion: The 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. Background The contribution of exposure to cigarette smoke (CS) to the development and progression of chronic obstructive pulmonary disease (COPD), cancer, and cardiovascular diseases is widely recognized [1, 2]. Electronic cigarettes (ECIGs) are commercially available since 2004, but patents for similar devices reach back to 1965 [3, 4]. 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. The flavors cover a broad range of tastes from fruit or spices, to different brands of tobacco. An intense scientific and political discussion about the toxicity and potential harm reduction of ECIGs is ongoing. 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]. Several studies have analyzed the effects of ECIGs on lung cells with the goal to evaluate toxic effects on cells and tissues [7]. A number of negative outcomes on different tissue culture systems (cell death, impaired repair, oxidative stress) have been reported [7-9]. In parallel, several ...

Sub-ohm vaping increases the levels of carbonyls, is cytotoxic, and alters gene expression in human bronchial epithelial cells exposed at the air–liquid interface

“…For instance, 7 different e-liquid flavoring chemicals induced significant IL-8 release from BEAS-2B and HFL-1 cells, while under the same exposure conditions, no significant IL-8 induction was observed in H292 cells [48]. In another study, while IL-8 concentration was significantly increased in Calu-3 cells exposed to e-cig aerosols at the ALI when compared to control cells, H292 cells and primary human bronchial epithelial cells did not significantly augment the synthesis of IL-8 from baseline control levels [80]. These results have at least two implications: 1) H292 cells and primary human lung epithelial cells may exhibit similar IL-8 release cellular responses after exposure to e-cig aerosols at the ALI; and 2) that in an ALI exposure model, H292 cells, although a cancer cell-line, may be a relevant surrogate for primary human bronchial epithelial cells, which are more complex and difficult to use reliably in large scale and long-term experimental ALI context.…”

Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

“…Nevertheless, our previous studies indicate that the permeability of epithelial monolayers increase only after repeated exposure to cigarettes, suggesting that disruption of permeability, as observed in this study, is in proportion to the length of the exposure [ 11 , 16 , 36 ]. Indeed, an absence of epithelial barrier disruption in in vitro models of very short exposures to EC has been reported [ 37 ]. In addition, flavors in the e-liquid may positively modulate permeability as well, which was previously shown in cell lines exposed to EC [ 38 ].…”

Pilot Study to Detect Genes Involved in DNA Damage and Cancer in Humans: Potential Biomarkers of Exposure to E-Cigarette Aerosols

“…DNA damage is usually corrected by the proofreading function of DNA polymerases that can recognize damaged sites in DNA; however, when a cell accumulates a large amount of DNA damage over a short time, its repair systems get saturated and replication occurs in cells with unrepaired lesions, leading to the perpetuation of mutations that can lead to cancer [ 25 ]. Efforts have been made to understand the gene expression profile after e-cig exposure [ 26 , 27 , 28 ]. Although informative, these studies either performed exposure assessment based on in vitro assays or did not account for the endogenous levels of the measured genes in vivo.…”