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Article

Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation

1
Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of California San Diego, La Jolla, CA 92093, USA
2
Research Service, VA San Diego Healthcare System San Diego, La Jolla, CA 92161, USA
3
Department of Radiology, Radiology Service, VA San Diego Healthcare System San Diego, University of California San Diego, La Jolla, CA 92093, USA
4
Department of Pathology, Pathology Service, VA San Diego Healthcare System San Diego, University of California San Diego, La Jolla, CA 92093, USA
*
Author to whom correspondence should be addressed.
Authors contributed equally.
Int. J. Mol. Sci. 2020, 21(15), 5513; https://doi.org/10.3390/ijms21155513
Received: 3 July 2020 / Revised: 27 July 2020 / Accepted: 27 July 2020 / Published: 31 July 2020
(This article belongs to the Section Molecular Informatics)
The COVID-19 pandemic caused by the SARS-CoV-2 virus, overlaps with the ongoing epidemics of cigarette smoking and electronic cigarette (e-cig) vaping. However, there is scarce data relating COVID-19 risks and outcome with cigarette or e-cig use. In this study, we mined three independent RNA expression datasets from smokers and vapers to understand the potential relationship between vaping/smoking and the dysregulation of key genes and pathways related to COVID-19. We found that smoking, but not vaping, upregulates ACE2, the cellular receptor that SARS-CoV-2 requires for infection. Both smoking and use of nicotine and flavor-containing e-cigs led to upregulation of pro-inflammatory cytokines and inflammasome-related genes. Specifically, chemokines including CCL20 and CXCL8 are upregulated in smokers, and CCL5 and CCR1 are upregulated in flavor/nicotine-containing e-cig users. We also found genes implicated in inflammasomes, such as CXCL1, CXCL2, NOD2, and ASC, to be upregulated in smokers and these e-cig users. Vaping flavor and nicotine-less e-cigs, however, did not lead to significant cytokine dysregulation and inflammasome activation. Release of inflammasome products, such as IL-1B, and cytokine storms are hallmarks of COVID-19 infection, especially in severe cases. Therefore, our findings demonstrated that smoking or vaping may critically exacerbate COVID-19-related inflammation or increase susceptibility to COVID-19. View Full-Text
Keywords: electronic cigarettes; vaping; COVID-19; SARS-CoV-2; ACE2; tobacco; inflammation; cytokines; immune response electronic cigarettes; vaping; COVID-19; SARS-CoV-2; ACE2; tobacco; inflammation; cytokines; immune response
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MDPI and ACS Style

Lee, A.C.; Chakladar, J.; Li, W.T.; Chen, C.; Chang, E.Y.; Wang-Rodriguez, J.; Ongkeko, W.M. Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation. Int. J. Mol. Sci. 2020, 21, 5513. https://doi.org/10.3390/ijms21155513

AMA Style

Lee AC, Chakladar J, Li WT, Chen C, Chang EY, Wang-Rodriguez J, Ongkeko WM. Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation. International Journal of Molecular Sciences. 2020; 21(15):5513. https://doi.org/10.3390/ijms21155513

Chicago/Turabian Style

Lee, Abby C., Jaideep Chakladar, Wei T. Li, Chengyu Chen, Eric Y. Chang, Jessica Wang-Rodriguez, and Weg M. Ongkeko 2020. "Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation" International Journal of Molecular Sciences 21, no. 15: 5513. https://doi.org/10.3390/ijms21155513

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