A study published in the European Respiratory Journal took a look into why current cigarette smokers and people with chronic obstructive pulmonary disease (COPD) could have an increased risk for severe COVID-19.
FRIDAY, April 17, 2020 (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.