Journal
CELL STEM CELL
Volume 27, Issue 6, Pages 869-+Publisher
CELL PRESS
DOI: 10.1016/j.stem.2020.11.010
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Funding
- NIH/NCI [R01CA208303]
- Tobacco-Related Disease Research Program (TRDRP) High Impact Pilot Research Award (HIPRA) [26IP-0036]
- TRDRP HIPRA [29IP-0597]
- UCOP Emergency Funding COVID19 TRDRP Seed grant Award [R00RG2383]
- Burroughs Wellcome Fund under the Innovation in Regulatory Science Award Program
- California Institute for Regenerative Medicine [DISC2COVID11764]
- Ablon Research Scholars Award
- UCLA Oversight COVID-19 Research Committee (OCRC)
- UCLA Eli & Edythe Broad Center of Regenerative Medicine and Stem Cell Research (BSCRC)
- UCLA Medical Scientist Training Program grant [NIH NIGMS GM008042]
- UCLA BSCRC
- David Geffen School of Medicine
- NIH [P01 GM099134]
- Howard Hughes Medical Institute
- NIH National Center for Advancing Translational Science (NCATS) UCLA CTSI [UL1TR001881]
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Current smoking is associated with increased risk of severe COVID-19, but it is not clear how cigarette smoke (CS) exposure affects SARS-CoV-2 airway cell infection. We directly exposed air-liquid interface (ALI) cultures derived from primary human nonsmoker airway basal stem cells (ABSCs) to short term CS and then infected them with SARS-CoV-2. We found an increase in the number of infected airway cells after CS exposure with a lack of ABSC proliferation. Single-cell profiling of the cultures showed that the normal interferon response was reduced after CS exposure with infection. Treatment of CS-exposed ALI cultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for more severe viral infection. Our data show that acute CS exposure allows for more severe airway epithelial disease from SARS-CoV-2 by reducing the innate immune response and ABSC proliferation and has implications for disease spread and severity in people exposed to CS.
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