TY -的T1 COVID-19和尼古丁作为调停者of ACE-2 JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/13993003.01261-2020 SP - 2001261 AU - Leung, Janice M. AU - Yang, Chen Xi AU - Sin, Don D. Y1 - 2020/01/01 UR - //www.qdcxjkg.com/content/early/2020/04/27/13993003.01261-2020.abstract N2 - We recently reported that current smokers and those with COPD had higher airway epithelial cell expression of the angiotensin-converting enzyme-2 (ACE-2) viral entry receptor [1]. We thus read with great interest the work of Russo et al. [2] which proposes a mechanism for this finding, namely that this upregulation is mediated by nicotine exposure specifically through the α7 subtype of nicotine acetylcholine receptors (α7-nAChR). While exposure to increasing concentrations of nicotine caused epithelial cells to increase ACE-2 levels, subsequent gene silencing of α7-nAChR appeared to significantly dampen this response. A secondary transcriptome sequencing analysis of our cohort (consisting of 42 subjects who underwent bronchoscopy for epithelial cell brushings [1]) reveals evidence in support of this hypothesis. We found that airway epithelial cell expression of CHRNA7, encoding α7-nAChR, was significantly correlated with the expression of ACE2 (fig. 1, Pearson r=0.54, p=2.31×10−8). There was significantly higher CHRNA7 expression in those with COPD (2.75±0.73 versus 2.14±0.43 in those without COPD, p=1.47×10−4), with a trend towards higher expression in current smokers compared to former and never smokers (2.86±0.92 in current smokers, 2.35±0.57 in former smokers, and 2.27±0.45 in never smokers, p=6.16×10−2). CHRNA7 was also negatively correlated with forced expiratory volume in 1 s percent predicted (Pearson r=−0.37, p=2.83×10−4). Interestingly, CHRNA7 was positively if weakly correlated with body mass index (Pearson r=0.14, p=6.31×10−3), raising the intriguing possibility that nicotine receptor mediation of ACE-2 may also be related to why obese individuals have made up a considerable proportion of COVID-19 cases [3]. α7-nAChR may upregulate ACE-2 ER -