Alveolar Epithelial Cell Dysfunction Induced By Flavored E-Cigarette Aerosols

Temple Univ Of The Commonwealth, Philadelphia PA

Investigators

Linked publications & trials

Abstract

Abstract E-cigarette devices produce an aerosol from e-liquids containing flavorings, nicotine, and vehicle. Inhaled e- cigarette aerosol can reach the alveolar region. Alveolar type II (ATII) cells produce and secrete pulmonary surfactant, which decreases surface tension. They also have a stem cell potential, proliferate and repair the epithelium after damage leading to lung regeneration. Due to their energy-demanding functions and location in the lung, they depend highly on mitochondria. Mitochondrial DNA lacks histones that serve as a barrier against damaging factors, contributing to its susceptibility to damage. Mitochondrial dysfunction can lead to mitophagy and ATII cell death. Our preliminary results in the parent R01 grant and this application demonstrate the harmful effect of e-cigarette aerosols with fruit and dessert flavors on human primary ATII cells. The goal of this administrative supplement proposal is to clarify further the sex influences on human primary ATII cell dysfunction caused by exposure to flavored constituents and e-cigarette aerosols. In Aim 1, we will compare DNA damage in ATII cells exposed to flavored constituents and e-cigarette aerosols with fruit and dessert flavors. In Aim 2, we will define the impact of this exposure on mitochondrial function in ATII cells. Obtained results will define sex influences on the respiratory injury risk of flavored constituents and e-cigarette aerosols.