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Original Research ARTICLE

Front. Pharmacol. | doi: 10.3389/fphar.2021.652102

Role of cigarette smoke on ACE-2 protein membrane expression in bronchial epithelial cells using an air-liquid interface model Provisionally accepted The final, formatted version of the article will be published soon. Notify me

 Massimo Caruso1, 2, Alfio Distefano1,  Rosalia Emma1,  Michelino Di Rosa3, Giuseppe Carota1, Sonja Rust2,  Riccardo Polosa2, 4,  Pietro Zuccarello5,  Margherita Ferrante2, 5, Giuseppina Raciti6 and  Giovanni Li Volti1, 2*
  • 1Section of Medical biochemistry, Department of Biomedical and Biotechnological Sciences, University of Catania, Italy
  • 2Center of Excellence for the acceleration of HArm Reduction, Department of Clinical and Experimental Medicine, University of Catania, Italy
  • 3Section of Human anatomy and histology, Department of Biomedical and Biotechnological Sciences, University of Catania, Italy
  • 4Department of Clinical and Experimental Medicine, University of Catania, Italy
  • 5Department of Medical, Surgical Sciences and Advanced Technologies G.F. Ingrassia, University of Catania, Italy
  • 6Department of Drug and Health Sciences, University of Catania, Italy

Prevalence studies of current smoking, among hospitalized COVID-19 patients, demonstrated an unexpectedly low prevalence among patients with COVID-19. The aim of the present study was to evaluate the effect of smoke from cigarettes on ACE-2 in bronchial epithelial cells. Normal bronchial epithelial cells (H292) were exposed to smoke by an air-liquid-interface (ALI) system and ACE-2 membrane protein expression was evaluated after 24 hours from exposure. Our transcriptomics data analysis showed a significant selective reduction of membrane ACE-2 expression (about 25%) following smoking exposure. Interestingly, we observed a positive direct correlation between ACE-2 reduction and nicotine delivery. Furthermore, by stratifying GSE52237 as a function of ACE-2 gene expression levels, we highlighted 1012 genes related to ACE-2 in smokers and 855 in non-smokers. Furthermore, we showed that 161 genes involved in the endocytosis process were highlighted using the online pathway tool KEGG. Finally, 11 genes were in common between the ACE-2 pathway in smokers and the genes regulated during endocytosis, while 12 genes with non-smokers. Interestingly, six in non-smokers and four genes in smokers were closely involved during the viral internalization process. Our data may offer a pharmaceutical role of nicotine as potential treatment option in COVID-19.

Keywords: ACE-2, Nicotine, Smoke, cigarette, Epithelial Cells

Received: 11 Jan 2021; Accepted: 05 Feb 2021.

Copyright: © 2021 Caruso, Distefano, Emma, Di Rosa, Carota, Rust, Polosa, Zuccarello, Ferrante, Raciti and Li Volti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Giovanni Li Volti, Section of Medical biochemistry, Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, 95123, Sicily, Italy, livolti@unict.it