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

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@article{d3bcf7a1330d44258b491bd7d9925c98,
title = "Understanding potential mechanisms of harm: the drivers of electronic cigarette-induced changes in alveolar macrophages, neutrophils and lung epithelial cells",
abstract = "Electronic 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 in vitro studies mimicking e-cigarette exposure aim to detect early indicators of harm. In response to e-cigarette exposure, alveolar macrophages adopt a pro-inflammatory phenotype of increased secretion of proinflammatory cytokines, reduction in phagocytosis and efferocytosis and reactive oxygen species generation. These effects are largely driven by free radical exposure, changes in PI3K/Akt signalling pathways, nicotine-induced reduction in phagocytosis receptors and impaired lipid homeostasis leading to a foam-like lipid laden phenotype. Neutrophils exhibit disrupted chemotaxis and transmigration to chemokines, reduced phagocytosis and bacterial killing and an increase in protease secretion without corresponding antiproteases in response to e-cigarette exposure. This is driven by an altered ability to respond and polarise towards chemoattractants, an activation of the p38 MAPK signalling pathway and inability to assemble NADPH oxidase. E-cigarettes induce lung epithelial cells to display decreased ciliary beat frequency and ion channel conductance ability as well as changes in chemokine secretion and surface protein expression. Changes in gene expression, mitochondrial function and signalling pathways have been demonstrated in lung epithelial cells to explain these changes. Many functional outputs of alveolar macrophages, neutrophils and lung epithelial cells have not yet been fully explored in the context of e-cigarette exposure, and the underlying driving mechanisms are poorly understood. This review discusses the current evidence surrounding the effects of e-cigarettes on alveolar macrophages, neutrophils and lung epithelial cells with particular focus on the cellular mechanisms of change.",
keywords = "e-cigarettes, neutrophils, alveolar macrophages, lung epithelial cells, mechanisms",
author = "Alice Jasper and Elizabeth Sapey and David Thickett and Aaron Scott",
year = "2021",
month = may,
day = "19",
doi = "10.1152/ajplung.00081.2021",
language = "English",
journal = "American journal of physiology. Lung cellular and molecular physiology",
issn = "1040-0605",
publisher = "American Physiological Society",

}

RIS

TY - JOUR

T1 - Understanding potential mechanisms of harm

T2 - the drivers of electronic cigarette-induced changes in alveolar macrophages, neutrophils and lung epithelial cells

AU - Jasper, Alice

AU - Sapey, Elizabeth

AU - Thickett, David

AU - Scott, Aaron

PY - 2021/5/19

Y1 - 2021/5/19

N2 - Electronic 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 in vitro studies mimicking e-cigarette exposure aim to detect early indicators of harm. In response to e-cigarette exposure, alveolar macrophages adopt a pro-inflammatory phenotype of increased secretion of proinflammatory cytokines, reduction in phagocytosis and efferocytosis and reactive oxygen species generation. These effects are largely driven by free radical exposure, changes in PI3K/Akt signalling pathways, nicotine-induced reduction in phagocytosis receptors and impaired lipid homeostasis leading to a foam-like lipid laden phenotype. Neutrophils exhibit disrupted chemotaxis and transmigration to chemokines, reduced phagocytosis and bacterial killing and an increase in protease secretion without corresponding antiproteases in response to e-cigarette exposure. This is driven by an altered ability to respond and polarise towards chemoattractants, an activation of the p38 MAPK signalling pathway and inability to assemble NADPH oxidase. E-cigarettes induce lung epithelial cells to display decreased ciliary beat frequency and ion channel conductance ability as well as changes in chemokine secretion and surface protein expression. Changes in gene expression, mitochondrial function and signalling pathways have been demonstrated in lung epithelial cells to explain these changes. Many functional outputs of alveolar macrophages, neutrophils and lung epithelial cells have not yet been fully explored in the context of e-cigarette exposure, and the underlying driving mechanisms are poorly understood. This review discusses the current evidence surrounding the effects of e-cigarettes on alveolar macrophages, neutrophils and lung epithelial cells with particular focus on the cellular mechanisms of change.

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

KW - e-cigarettes

KW - neutrophils

KW - alveolar macrophages

KW - lung epithelial cells

KW - mechanisms

U2 - 10.1152/ajplung.00081.2021

DO - 10.1152/ajplung.00081.2021

M3 - Review article

JO - American journal of physiology. Lung cellular and molecular physiology

JF - American journal of physiology. Lung cellular and molecular physiology

SN - 1040-0605

ER -