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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)

Citation

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, 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, 10, (5) pp. 1-18. ISSN 2077-0383 (2021) [Refereed Article]


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DOI: doi:10.3390/jcm10051028

Abstract

Tobacco smoking has emerged as a risk factor for increasing the susceptibility to infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via increased expression of angiotensin-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 increase susceptibility to SARS-CoV-2 infection. We exposed BEAS-2B cells (bronchial epithelium transformed with Ad12-SV40 2B) and primary small airway epithelial cells (SAECs) to electronic cigarette aerosol condensates produced from propylene glycol/vegetable glycerin or commercially bought e-liquid (ħadded nicotine) and cigarette smoke extract to investigate if electronic cigarette exposure, like cigarette 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) were measured for both 4- and 24 h treatments in BEAS-2B cells and 4 h in SAECs; ACE2 gene expression was measured using quantitative polymerase chain reaction (qPCR) for 4 h treatment in BEAS-2B cells. Nicotine-free condensates and higher concentrations of nicotine-containing condensates were cytotoxic to BEAS-2B cells. Higher LDH release and reduced membrane integrity were seen in BEAS-2B cells treated for 24 h with higher concentrations of nicotine-containing condensates. ACE2 protein expression was observably increased in all treatments compared to cell controls, particularly for 24 h exposures. ACE2 gene expression was significantly increased in cells exposed to the locally bought e-liquid condensate with high nicotine concentration and cigarette smoke extract compared with cell controls. Our study suggests that vaping alone and smoking alone can result in an increase in lung ACE2 expression. Vaping and smoking are avoidable risk factors for COVID-19, which, if avoided, could help reduce the number of COVID-19 cases and the severity of the disease. This is the first study to utilize electronic cigarette aerosol condensates, novel and developed in our laboratory, for investigating ACE2 expression in human airway epithelial cells.

Item Details

Item Type:Refereed Article
Keywords:COVID-19, vaping, COPD, infections, electronic cigarettes, SARS-CoV-2
Research Division:Biomedical and Clinical Sciences
Research Group:Cardiovascular medicine and haematology
Research Field:Cardiology (incl. cardiovascular diseases)
Objective Division:Health
Objective Group:Clinical health
Objective Field:Diagnosis of human diseases and conditions
UTAS Author:McAlinden, KD (Mr Kielan McAlinden)
UTAS Author:LU, W (Dr Monica LU)
UTAS Author:Vahidi Ferdowsi, P (Ms Parisa Vahidi Ferdowsi)
UTAS Author:Myers, S (Dr Stephen Myers)
UTAS Author:Markos, J (Dr Jim Markos)
UTAS Author:Larby, J (Dr Josie Larby)
UTAS Author:Weber, HC (Dr Heinrich Weber)
UTAS Author:Haug, G (Dr Greg Haug)
UTAS Author:Eapen, MS (Mr Mathew Eapen)
UTAS Author:Sohal, SS (Dr Sukhwinder Sohal)
ID Code:145261
Year Published:2021
Web of Science® Times Cited:3
Deposited By:Health Sciences
Deposited On:2021-07-14
Last Modified:2021-07-15
Downloads:0

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