ACE-2 expression in the small airway epithelia of smokers and COPD patients: implications for COVID-19

Abstract

Smokers and those with COPD have increased airway expression of ACE-2, which is the entry receptor for the COVID-19 virus. This may explain the increased risk of severe COVID-19 in these subpopulations and highlight the importance of smoking cessation. https://bit.ly/3bC29es

FIGURE 1

a) A violin plot of angiotensin-converting enzyme II (ACE-2) expression the in small airways of COPD and non-COPD subjects in the St Paul's Hospital (Vancouver, BC, Canada) cohort. The red box indicates the median and interquartile range. The p-value was obtained using a robust linear model. b) A scatterplot of ACE-2 expression in the small airways according to forced expiratory volume in 1 s (FEV₁) % predicted in the St Paul's Hospital cohort. ACE-2 gene expression in airway epithelia is inversely related to FEV₁ % pred (p=0.0348). c) A violin plot of ACE-2 expression in the small airways of never-, former and current smokers in the St Paul's Hospital cohort. The red box indicates the median and the interquartile range. The p-value was obtained using a robust linear model. d) Protein staining of ACE-2 in the airways of individuals with and without COPD. A human kidney slide was the positive control for ACE-2. The specificity of the antibody against ACE-2 was determined using an immunoblot assay with HEK2 cell lysates as a positive control. The expected molecular weight of ACE-2 is 90–100 kDa. In the airways, most of the protein expression was noted in the epithelial layer, and most pronounced in those with COPD. CPM: counts per million; NHBE: normal human bronchial epithelial cells.