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Electronic cigarette aerosol is cytotoxic and increases ACE2 expression on human airway epithelial cells: Implications for SARS-CoV-2 (COVID-19)


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McAlinden, KD, LU, W ORCID: 0000-0003-1550-2276, Vahidi Ferdowsi, P, Myers, S ORCID: 0000-0003-4793-3820, Markos, J, Larby, J, Chia, C, Weber, HC, Haug, G, Eapen, MS ORCID: 0000-0003-0570-7059 and Sohal, SS ORCID: 0000-0001-9627-6498 2021 , 'Electronic cigarette aerosol is cytotoxic and increases ACE2 expression on human airway epithelial cells: Implications for SARS-CoV-2 (COVID-19)' , Journal of Clinical Medicine, vol. 10, no. 5 , pp. 1-18 , doi: 10.3390/jcm10051028.

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Tobacco smoking has emerged as a risk factor for increasing the susceptibility to infectionfrom severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via increased expression ofangiotensin-converting enzyme-2 (ACE2) in the lung, linked to coronavirus disease 2019 (COVID-19)development. Given the modifiable nature of electronic cigarettes and the delivery of high concentrations of nicotine, we investigate whether electronic cigarette vaping has the potential to increasesusceptibility to SARS-CoV-2 infection. We exposed BEAS-2B cells (bronchial epithelium transformedwith Ad12-SV40 2B) and primary small airway epithelial cells (SAECs) to electronic cigarette aerosolcondensates produced from propylene glycol/vegetable glycerin or commercially bought e-liquid(±added nicotine) and cigarette smoke extract to investigate if electronic cigarette exposure, likecigarette smoke, increases the expression of ACE2 in lung epithelial cells. In BEAS-2B cells, cytotoxicity (CCK-8), membrane integrity (LDH), and ACE2 protein expression (immunofluorescence) weremeasured for both 4- and 24 h treatments in BEAS-2B cells and 4 h in SAECs; ACE2 gene expressionwas measured using quantitative polymerase chain reaction (qPCR) for 4 h treatment in BEAS-2Bcells. Nicotine-free condensates and higher concentrations of nicotine-containing condensates werecytotoxic to BEAS-2B cells. Higher LDH release and reduced membrane integrity were seen inBEAS-2B cells treated for 24 h with higher concentrations of nicotine-containing condensates. ACE2protein expression was observably increased in all treatments compared to cell controls, particularlyfor 24 h exposures. ACE2 gene expression was significantly increased in cells exposed to the locallybought e-liquid condensate with high nicotine concentration and cigarette smoke extract comparedwith cell controls. Our study suggests that vaping alone and smoking alone can result in an increasein lung ACE2 expression. Vaping and smoking are avoidable risk factors for COVID-19, which, ifavoided, could help reduce the number of COVID-19 cases and the severity of the disease. This is thefirst study to utilize electronic cigarette aerosol condensates, novel and developed in our laboratory,for investigating ACE2 expression in human airway epithelial cells.

Item Type: Article
Authors/Creators:McAlinden, KD and LU, W and Vahidi Ferdowsi, P and Myers, S and Markos, J and Larby, J and Chia, C and Weber, HC and Haug, G and Eapen, MS and Sohal, SS
Keywords: COVID-19, vaping, COPD, infections, electronic cigarettes, SARS-CoV-2
Journal or Publication Title: Journal of Clinical Medicine
Publisher: MDPI AG
ISSN: 2077-0383
DOI / ID Number: 10.3390/jcm10051028
Copyright Information:

Copyright 2021 the authors.Licensee MDPI, Basel, Switzerland.This article is an open access articledistributed under the terms andconditions of the Creative CommonsAttribution (CC BY) license (

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