Nicotine upregulates ACE2 expression and increases competence for SARS-CoV-2 in human pneumocytes. Issue 2 (12th April 2021)

• Record Type: Journal Article
• Authors: Maggi, Fabrizio; Rosellini, Alfredo; Spezia, Pietro Giorgio; Focosi, Daniele; Macera, Lisa; Lai, Michele; Pistello, Mauro; de Iure, Antonio; Tomino, Carlo; Bonassi, Stefano; Russo, Patrizia
• Is Part Of: ERJ open research. Volume 7:Issue 2(2021)
• Publication Date: 2021-04-12
• Subjects: Respiratory organs -- Diseases -- Periodicals; Respiration -- Periodicals; Respiration; Respiratory organs -- Diseases; Respiratory organs -- Diseases -- Treatment; Respiratory Tract Diseases; Electronic journals; Fulltext; Internet Resources; Periodicals; Periodical; 616.2005
• DOI: 10.1183/23120541.00713-2020
• Languages: English
• ISSNs: 2312-0541

Abstract

The coronavirus disease 2019 (COVID-19) pandemic has a variable degree of severity according to underlying comorbidities and life-style. Several research groups have reported an association between cigarette smoking and increased severity of COVID-19. The exact mechanism of action is largely unclear. We exposed low angiotensin-converting enzyme 2 (ACE2)-expressing human pulmonary adenocarcinoma A549 epithelial cells to nicotine and assessed ACE2 expression at different times. We further used the nicotine-exposed cells in a virus neutralisation assay. Nicotine exposure induces rapid and long-lasting increases in gene and protein expression of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor ACE2, which in turn translates into increased competence for SARS-CoV-2 replication and cytopathic effect. These findings show that nicotine worsens SARS-CoV-2 pulmonary infection and have implications for public health policies. Nicotine, the psychotropic substance of tobacco, in human lung adenocarcinoma A549 cells, induces increased gene and protein expression of the #SARSCoV2 receptor ACE2, which in turn translates into high SARS-CoV-2 replication and cytopathic effect https://bit.ly/36njkA9