학술논문

E-cigarette vape and lung ACE2 expression: Implications for coronavirus vulnerability
Document Type
article
Source
Subject
Pharmacology and Pharmaceutical Sciences
Biomedical and Clinical Sciences
Infectious Diseases
Tobacco
Tobacco Smoke and Health
Lung
Prevention
Aetiology
2.2 Factors relating to the physical environment
Respiratory
Good Health and Well Being
Angiotensin-Converting Enzyme 2
Animals
COVID-19
DNA
Complementary
Electronic Nicotine Delivery Systems
Female
Male
Mice
Mice
Inbred C57BL
Nicotine
Nicotinic Agonists
Receptors
Nicotinic
Sex Characteristics
Vaping
alpha7 Nicotinic Acetylcholine Receptor
E-cigarette
ACE2
Individual differences
Environmental Science and Management
Toxicology
Pharmacology and pharmaceutical sciences
Environmental management
Pollution and contamination
Language
Abstract
Evidence in humans suggests a correlation between nicotine smoking and severe respiratory symptoms with COVID-19 infection. In lung tissue, angiotensin-converting enzyme 2 (ACE2) appears to mechanistically underlie viral entry. Here, we investigated whether e-cigarette vapor inhalation alters ACE2 and nicotinic acetylcholine receptor (nAChR) expression in male and female mice. In male lung, nicotine vapor inhalation induced a significant increase in ACE2 mRNA and protein, but surprisingly, these differences were not found in females. Further, both vehicle and nicotine vapor inhalation downregulated α5 nAChR subunits in both sexes, while differences were not found in α7 nAChR subunit expression. Finally, blood ACE2 levels did not differ with exposure, indicating that blood sampling is not a sufficient indicator of lung ACE2 changes. Together, these data indicate a direct link between e-cigarette vaping and increased ACE2 expression in male lung tissue, which thereby reveals an underlying mechanism of increased vulnerability to coronavirus infection in individuals vaping nicotine.