Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells.

Introduction:
This article is a research study that compares the acute effects of traditional cigarettes (TCIGs) and electronic cigarettes (ECIGs) on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (phBE). The study used an in vitro TCIG-exposure model and adapted it to the vaporization of ECIG-liquid, normalized the amount of ECIG-vapor to the content of nicotine from the established TCIG-exposure model, and chose nicotine consumption as a normalization factor to account for the needs of smokers to meet their demands for nicotine when switching between TCIGs and ECIGs.

Key Points:

* The study found that bacterial killing, barrier integrity, and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples.
* TCIGs negatively affected host defense and reduced barrier integrity in a significant way.
* 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.
* ECIGs have a very different expression pattern compared to TCIG and control samples, whereas the ECIG and controls can also be clearly separated but show a more similar expression pattern.
* The exposure of differentiated airway epithelium to ECIG-vapor caused a decrease of antibacterial host defense and increased biofilm formation.
* ECIG use was associated with decreased expression of immune-related genes and the application of ECIG-fluid, not vapor, to primary epithelial cells resulted in increased inflammation and susceptibility to virus infection.

Main Message:
The main message of the study is that ECIGs impact on the biology of airway epithelial cells with the release of inflammatory mediators but no overt reduction of antibacterial host defense. The acute toxic effect of ECIGs appeared to be less as compared to TCIG-exposure. however, the study suggests that ECIGs may not be entirely harmless, as they can cause an increase in inflammation and impair the barrier function of airway epithelial cells. The study also highlights the need for further research to fully understand the long-term effects of ECIG use.

herr C, Tsitouras K, Niederstraßer J, et al. Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells. Respiratory research. 2020;21(1):67. doi:10.1186/s12931-020-1317-2