Type 2 inflammation modulates ACE2 and TMPRSS2 in airway epithelial cells - 22/07/20
Abstract |
Background |
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has dramatically changed our world, country, communities, and families. There is controversy regarding risk factors for severe COVID-19 disease. It has been suggested that asthma and allergy are not highly represented as comorbid conditions associated with COVID-19.
Objective |
Our aim was to extend our work in IL-13 biology to determine whether airway epithelial cell expression of 2 key mediators critical for SARS-CoV-2 infection, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2), are modulated by IL-13.
Methods |
We determined effects of IL-13 treatment on ACE2 and TMPRSS2 expression ex vivo in primary airway epithelial cells from participants with and without type 2 asthma obtained by bronchoscopy. We also examined expression of ACE2 and TMPRSS2 in 2 data sets containing gene expression data from nasal and airway epithelial cells from children and adults with asthma and allergic rhinitis.
Results |
IL-13 significantly reduced ACE2 and increased TMPRSS2 expression ex vivo in airway epithelial cells. In 2 independent data sets, ACE2 expression was significantly reduced and TMPRSS2 expression was significantly increased in the nasal and airway epithelial cells in type 2 asthma and allergic rhinitis. ACE2 expression was significantly negatively associated with type 2 cytokines, whereas TMPRSS2 expression was significantly positively associated with type 2 cytokines.
Conclusion |
IL-13 modulates ACE2 and TMPRSS2 expression in airway epithelial cells in asthma and atopy. This deserves further study with regard to any effects that asthma and atopy may render in the setting of COVID-19 infection.
Le texte complet de cet article est disponible en PDF.Key words : Asthma, IL-13, ACE2, TMPRSS2, nasal epithelial cells, airway epithelial cells, COVID-19, SARS-CoV-2, type 2 inflammation
Abbreviations used : ACE2, Ang I, Ang II, CLCA1, FVC, POSTN, PPIA, SARS-CoV-2, SERPINB2, TMPRSS2
Plan
| Supported by a National Institutes of Health Funding (grant U19AI125357); an Arizona Bioscience Research Grant (to M.K.); and the MSD Life Science Foundation, Public Interest Incorporated Foundation (to H.K.). |
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| Disclosure of potential conflict of interest: H. Kimura has received grants from MSD Life Science Foundation outside the submitted work. F. Martinez has received grants from the National Institutes of Health (NIH)/National Heart, Lung and Blood Institute, the NIH/National Institute of Environmental Health Sciences, the NIH/National Institute of Allergy and Infectious Diseases, the NIH/Office of the Director, and Johnson & Johnson, as well as consulting fees from Copeval and Commense outside the submitted work. M. Kraft has received grants from the NIH/National Heart, Lung and Blood Institute, Sanofi, ALA, Chiesi, and AstraZeneca; royalties from Elsevier; and consulting fees from AstraZeneca and Sanofi outside the submitted work. The rest of the authors declare that they have no conflicts of interest. |
Vol 146 - N° 1
P. 80 - juillet 2020 Retour au numéro
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