Understanding potential mechanisms of harm: the drivers of electronic cigarette-induced changes in alveolar macrophages, neutrophils, and lung epithelial cells

Electronic (e-) cigarettes are growing in popularity despite uncertainties regarding their long-term health implications. The link between cigarette smoking and initiation of chronic lung disease took decades to unpick so vitro studies mimicking e-cigarette exposure aim detect early indicators harm. In response exposure, alveolar macrophages adopt a proinflammatory phenotype increased secretion cytokines, reduction phagocytosis, efferocytosis reactive oxygen species generation. These effects largely driven by free radical changes PI3K/Akt signaling pathways, nicotine-induced phagocytosis receptors, impaired lipid homeostasis leading foam-like lipid-laden phenotype. Neutrophils exhibit disrupted chemotaxis transmigration chemokines, reduced bacterial killing, an increase protease without corresponding antiproteases exposure. This is altered ability respond polarize toward chemoattractants, activation the p38 MAPK pathway inability assemble NADPH oxidase. E-cigarettes induce epithelial cells display decreased ciliary beat frequency ion channel conductance as well chemokine surface protein expression. Changes gene expression, mitochondrial function, pathways have been demonstrated explain these changes. Many functional outputs macrophages, neutrophils, not fully explored context underlying driving mechanisms poorly understood. review discusses current evidence surrounding e-cigarettes on with particular focus cellular change.