Cigarette Smoke Exposure and Inflammatory Signaling Increase the Expression of the SARS-CoV-2 Receptor ACE2 in the Respiratory Tract

• Published in: Developmental cell Vol. 53; no. 5; pp. 514 - 529.e3
• Main Authors: Smith, Joan C., Sausville, Erin L., Girish, Vishruth, Yuan, Monet Lou, Vasudevan, Anand, John, Kristen M., Sheltzer, Jason M.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 08.06.2020
• Subjects: ACE2; Adult; Aged; Alveolar Epithelial Cells - metabolism; Angiotensin-Converting Enzyme 2; Animals; Caco-2 Cells; Cells, Cultured; Coronavirus; Coronavirus Infections - epidemiology; COVID-19; Female; HCT116 Cells; Humans; inflammation; interferon; Interferons - genetics; Interferons - metabolism; lung development; Male; Mice; Middle Aged; Pandemics; Peptidyl-Dipeptidase A - genetics; Peptidyl-Dipeptidase A - metabolism; Pneumonia, Viral - epidemiology; Rats; Respiratory Mucosa - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA-Seq; SARS-CoV-2; Signal Transduction; Single-Cell Analysis; smoking; Tobacco Smoke Pollution - adverse effects; Tobacco Smoking - epidemiology; Tobacco Smoking - genetics; Tobacco Smoking - metabolism; Up-Regulation; COVID-19; ACE2; SARS-CoV-2; Coronavirus; inflammation; smoking; interferon; lung development

The factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2...