ACE-2 Expression in the Small Airway Epithelia of Smokers and COPD Patients: Implications for COVID-19

Janice M Leung; Chen Xi Yang; Anthony Tam; Tawimas Shaipanich; Tillie L Hackett; Gurpreet K Singhera; Delbert R Dorscheid; Don D Sin

Robust linear models were used to determine whether 1) ACE-2 was differentially expressed in patients with COPD and in smokers after adjustment for age and sex and 2) ACE-2 expression was significantly correlated with lung function. All analyses were performed in R (version 3.5.0). In the immunohistochemistry dataset, Kruskal-Wallis test with Dunn's Multiple Comparisons test was used. Table 1 displays the demographic and clinical characteristics of the SPH cohort. ACE-2 expression in the epithelial cells was significantly increased in COPD versus non-COPD subjects (Mean±SD of non-COPD=1.70±0.51 versus COPD=2.52±0.66, p=7.62×10 -4 ; Figure 1A ). There was a significant inverse relationship between ACE-2 gene expression and FEV1% of predicted (r=-0.24; p=0.035; Figure 1B) . Interestingly, smoking status was also significantly related to ACE-2 gene expression levels in airways of these participants with current smokers having a significantly higher gene expression than never smokers (never smokers=1.78±0.39 versus current smokers=2.77±0.91, p=0.024). Former smokers had gene expression levels in-between that of never and current smokers (former smokers=2.00±1.23; Figure 1C ). Conditional on the smoking status, the association between ACE-2 expression and COPD was still significant (Adjusted Mean±SE of non-COPD: 0.90±0.65 versus COPD: 1.75±0.82, p=0.016).