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. 2020 May 14;55(5):2000688.
doi: 10.1183/13993003.00688-2020. Print 2020 May.

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

Janice M Leung  1   2   3 , Chen X Yang  1   2   3 , Anthony Tam  1   2   3 , Tawimas Shaipanich  2   3 , Tillie-Louise Hackett  2   3   4 , Gurpreet K Singhera  1   2   3 , Delbert R Dorscheid  1   2   3 , Don D Sin  5   2   3
Affiliations

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

Janice M Leung et al. Eur Respir J. .

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

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Conflict of interest statement

Conflict of interest: J.M. Leung has nothing to disclose. Conflict of interest: C.X. Yang has nothing to disclose. Conflict of interest: A. Tam has nothing to disclose. Conflict of interest: T. Shaipanich has nothing to disclose. Conflict of interest: T.L. Hackett has nothing to disclose. Conflict of interest: G.K. Singhera has nothing to disclose. Conflict of interest: D.R. Dorschied has nothing to disclose. Conflict of interest: D.D. Sin reports grants from Merck, personal fees for advisory board work from Sanofi-Aventis and Regeneron, grants and personal fees for research from Boehringer Ingelheim, grants and personal fees for advisory board work and lectures from AstraZeneca, personal fees for advisory board work and lectures from Novartis, outside the submitted work.

Figures

FIGURE 1
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.
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References

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