HealthDay News — Active cigarette smokers and individuals with chronic obstructive pulmonary disease (COPD) have up-regulation of angiotensin converting enzyme II (ACE-2) expression in the lower airways, which could explain the increased risk for severe COVID-19 in these subpopulations, according to a study published online April 8 in the European Respiratory Journal.

Noting that severe acute respiratory syndrome coronavirus-2 uses ACE-2 as the cellular entry receptor, Janice M. Leung, M.D., from the University of British Columbia in Vancouver, Canada, and colleagues examined ACE-2 expression in bronchial epithelial cells in the lower respiratory tract in patients with COPD compared to controls. Data were included for a cohort with 21 patients and 21 controls.

The researchers found that patients with COPD had lower forced expiratory volume in one second (FEV1) percent of predicted and FEV1/forced vital capacity compared with controls. In COPD versus non-COPD patients, ACE-2 expression in the epithelial cells was significantly increased. A significant inverse relationship was seen between ACE-2 gene expression and FEV1 percent of predicted. There was also a significant association seen between smoking status and ACE-2 gene expression levels in airways; current smokers had a significantly higher gene expression than never smokers. Gene expression levels of former smokers were in between those of never and current smokers. The association between ACE-2 expression and COPD was still significant, conditional on the smoking status. These findings were validated in two additional cohorts.

“These findings highlight the importance of smoking cessation for these individuals and increased surveillance of these risk subgroups for prevention and rapid diagnosis of this potentially deadly disease,” the authors write.


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One author disclosed financial ties to the pharmaceutical industry.

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