Modifications in MUC2 and OCLN Expression in Human Alveolar Adenocarcinoma Epithelial Cells Following E‐Cigarette Chemical Exposure

Abstract

Electronic cigarettes (e‐cigarettes) have entered the market promoting a healthy and clean alternative to conventional tobacco cigarettes. Aggressive marketing has led to an increase in usage of e‐cigarettes among adults and adolescents. Despite the promotion of e‐cigarettes as an alternative for tobacco users, the chemical composition of these two products is very similar. Two of the predominant chemicals found in e‐cigarettes are formalin and methylbenzaldehyde, of which, formalin is also found in tobacco cigarettes. We hypothesize that exposure of the alveolar adenocarcinoma (A549) cells to these common e‐cigarette chemicals will alter the lung epithelial barrier as measured by occludin (OCLN) and mucin‐2 (MUC2) expression.Mucin‐2 is a protein that secretes a protective mucus membrane and occludin is a tight junction protein, both contributing to a functional and protective lung epithelial barrier. Overexpression of MUC2 can lead to hypersecretion of mucus, while under expression of OCLN can cause an increase in epithelial permeability, representing a disruption of this barrier. A549 cells will be treated with physiological concentrations of formalin and methylbenzaldehyde to mimic e‐cigarette exposure. We will show that exposure to formalin and methylbenzaldehyde alters MUC2 and OCLN, indicating a disruption of the lung epithelial barrier. These results represent the negative health effects associated with e‐cigarette use, which contradicts the current advertisements marketing e‐cigarettes as a safe product.Support or Funding InformationNational Science Foundation Grant# 1458212This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.