PT  - JOURNAL ARTICLE
AU  - Valentino Bezzerri
AU  - Valentina Gentili
AU  - Martina Api
AU  - Alessia Finotti
AU  - Chiara Papi
AU  - Anna Tamanini
AU  - Debora Olioso
AU  - Martina Duca
AU  - Erika Tedesco
AU  - Sara Leo
AU  - Monica Borgatti
AU  - Sonia Volpi
AU  - Paolo Pinton
AU  - Giulio Cabrini
AU  - Roberto Gambari
AU  - Francesco Blasi
AU  - Giuseppe Lippi
AU  - Alessandro Rimessi
AU  - Roberta Rizzo
AU  - Marco Cipolli
TI  - ACE2 expression and localization are regulated by CFTR: implications beyond cystic fibrosis
AID  - 10.1101/2021.11.19.469220
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.11.19.469220
4099  - http://biorxiv.org/content/early/2021/11/22/2021.11.19.469220.short
4100  - http://biorxiv.org/content/early/2021/11/22/2021.11.19.469220.full
AB  - As an inherited disorder characterized by severe pulmonary disease, cystic fibrosis (CF) could be considered a comorbidity for coronavirus disease 2019 (COVID-19)1. Instead, CF seems to constitute an advantage in COVID-19 infection2-5.To clarify whether host factors expressed by the CF epithelia may influence COVID-19 progression, we investigated the expression of SARS-CoV-2 receptor and coreceptors in primary airway epithelial cells. We found that angiotensin converting enzyme 2 (ACE2) expression and localization are regulated by cystic fibrosis transmembrane conductance regulator (CFTR) channels. Consistently, our results indicate that dysfunctional CFTR channels alter susceptibility to SARS-CoV-2 infection, resulting in reduced viral infection in CF cells. Depending on the pattern of ACE2 expression, the SARS-CoV-2 spike (S) protein induced high levels of Interleukin (IL)-6 in healthy donor-derived primary airway epithelial cells but a very weak response in primary CF cells. Collectively, these data support the hypothesis that CF condition is unfavorable for SARS-CoV-2 infection.Competing Interest StatementThe authors have declared no competing interest.