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J Clin Invest. 2019 Sep 4. pii: 128531. doi: 10.1172/JCI128531. [Epub ahead of print]

Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine.

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Department of Medicine.
Interdepartmental Program in Translational Biology and Molecular Medicine.
Department of Pathology and Immunology.
Department of Molecular and Cell Biology.
Department of Psychiatry, and.
Department of Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Department of Integrative Biology and Molecular Pharmacology, University of Texas Health Science Center, Houston, Texas, USA.
Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico, Albuquerque, New Mexico, USA.
Biology of Inflammation Center, Baylor College of Medicine, Houston, Texas, USA.
Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, Texas, USA.


Electronic nicotine delivery systems (ENDS) or e-cigarettes have emerged as a popular recreational tool among adolescents and adults. Although the use of ENDS is often promoted as a safer alternative to conventional cigarettes, few comprehensive studies have assessed the long-term effects of vaporized nicotine and its associated solvents, propylene glycol (PG) and vegetable glycerin (VG). Here, we show that compared with smoke exposure, mice receiving ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema. However, ENDS exposure, independent of nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells. Comprehensive lipidomic and structural analyses of the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated phospholipids in the airway. In addition to ENDS-induced lipid deposition, chronic ENDS vapor exposure downregulated innate immunity against viral pathogens in resident macrophages. Moreover, independent of nicotine, ENDS-exposed mice infected with influenza demonstrated enhanced lung inflammation and tissue damage. Together, our findings reveal that chronic e-cigarette vapor aberrantly alters the physiology of lung epithelial cells and resident immune cells and promotes poor response to infectious challenge. Notably, alterations in lipid homeostasis and immune impairment are independent of nicotine, thereby warranting more extensive investigations of the vehicle solvents used in e-cigarettes.


Immunology; Inflammation; Innate immunity

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