Abstract
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.
Highlights
The current COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has killed over 130,000 Americans in less than 4 months
On the other hand, smoking e-cigarettes does not lead to increased ACE2 expression in either study (Figure 1B). These results suggest that tobacco smokers may be more vulnerable to SARS-CoV-2 infection than e-cigarette smokers if infection susceptibility is based upon ACE2 abundance
We discovered that many key inflammasome genes and regulators besides IL-1B were upregulated in smokers vs. former smokers, including CXCL1 and CXCL2 (Figure 3)
Summary
The current COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has killed over 130,000 Americans in less than 4 months. Current data indicate that patients who have cardiovascular and chronic respiratory conditions, including those caused by tobacco use, are at higher risk of developing severe COVID-19 symptoms and have significantly increased fatality [1]. Flavors and nicotine in e-cigs are frequently associated with more inflammation, epithelial barrier dysregulation, oxidative stress, and DNA damage than e-cigs with only basic components [12,13]. Another possible mechanism linking tobacco smoking to COVID-19 is its propensity to increase lung inflammation. Cigarette smoke has been associated with increased susceptibility to COVID-19 [17], the effect of tobacco on the immune response to SARS-CoV-2 has not been studied. Given that nicotine or flavorings present in the e-cig mixture are implicated in promoting lung damage, we examined one e-cig dataset where all participants only vaped e-cigs with neither nicotine nor flavors and another e-cig dataset where participants only vaped e-cigs with nicotine and were free to choose different flavors
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
