Effects of electronic cigarette aerosol on isolated murine lung cells and bronchoalveolar lavage fluid

Electronic cigarettes (e-cigarettes) are gaining popularity as an alternative to smoking, despite many unsolved questions regarding their safety. This study aimed to investigate effects of e-cigarette vapour extract (ECVE) and e-cigarette aerosol (ECA) on different pulmonary cell types or bronchoalveolar lavage fluid (BALF) from control mice or mice exposed to ECA, respectively. Primary isolated murine alveolar epithelial typeII cells (mAECII) and pulmonary arterial smooth muscle cells (mPASMC) were exposed to ECVE (containing 0mg/ml or 18mg/ml nicotine). We determined proliferation and migration in mPASMC, and performed whole genome expression analysis in mAECII and mPASMC. Additionally, flow cytometry was applied to characterize cellular composition of BALF from C57BL/6J mice exposed to ECA for 8 months. ECVE with and without nicotine inhibited cellular migration, but not proliferation in mPASMC and increased expression of inflammatory proteins, such as inducible nitric oxide synthase. Microarray data further revealed alteration of lysosomal and metabolic pathways, particularly glycolysis/gluconeogenesis in mPASMC. In contrast, metabolic pathways, particularly genes involved in cytochrome P450 and glutathione metabolism were upregulated in mAECII. Furthermore, the percentage of lymphocytes, neutrophils and alveolar exudate macrophages were increased, whereas resident alveolar macrophages were decreased in the BALF from mice exposed to ECA with or without nicotine compared to control groups. These results indicate that ECVE with and without nicotine alters cellular functions and intracellular pathways of mPASMC and mAECII. Moreover, ECA causes inflammatory responses in the lung.