Increased expression of ACE2, the SARS-CoV-2 entry receptor, in alveolar and bronchial epithelium of smokers and COPD subjects

Abstract

This study demonstrates increased protein levels of ACE2 in alveolar and bronchial epithelium of smokers and subjects with COPD, which might facilitate host cell entry of SARS-CoV-2 https://bit.ly/2ZazOrd

FIGURE 1

Gene and protein expression of angiotensin-converting enzyme 2 (ACE2) in the airways and lungs. a) ACE2 mRNA expression is increased in the lung tissue of smokers and COPD subjects. ACE2 mRNA expression in the lung tissue of never-, current and ex-smokers without airflow limitation and current and ex-smokers with moderate (Global Initiative of Chronic Obstructive Lung Disease (GOLD) stage II) or severe-to-very severe (GOLD stage III–IV) COPD, normalised to the expression of the housekeeping controls glyceraldehyde-3-phosphate dehydrogenase, peptidylprolyl isomerase A and succinate dehydrogenase complex flavoprotein subunit A. b) ACE2 protein levels are increased in the alveolar tissue of smokers and COPD subjects. Representative images and quantification of ACE2 immunohistochemical staining in the alveolar tissue of never-smokers, smokers without airflow limitation, smokers with COPD GOLD stage II and smokers with COPD GOLD stage III–IV. The area of ACE2-positive signal was normalised to the total area of alveolar tissue present in each analysed image. c) ACE2 protein levels are increased in the bronchial epithelium of smokers and COPD subjects. Representative images and quantification of ACE2 immunohistochemical staining in the bronchial epithelium of never-smokers, smokers without airflow limitation and smokers with COPD (GOLD stages II and III–IV). The area of ACE2-positive signal in each airway was normalised to the length of the basement membrane (Pbm). Data are presented as means±sem. *: p<0.05; **: p<0.01; ***: p<0.001.