Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Department of Pathology, McGill University, Montreal, Quebec, Canada.
Am J Physiol Lung Cell Mol Physiol. 2021 Jan 1;320(1):L152-L157. doi: 10.1152/ajplung.00455.2020. Epub 2020 Oct 28.
The COVID-19 pandemic is associated with severe pneumonia and acute respiratory distress syndrome leading to death in susceptible individuals. For those who recover, post-COVID-19 complications may include development of pulmonary fibrosis. Factors contributing to disease severity or development of complications are not known. Using computational analysis with experimental data, we report that idiopathic pulmonary fibrosis (IPF)- and chronic obstructive pulmonary disease (COPD)-derived lung fibroblasts express higher levels of angiotensin-converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 entry and part of the renin-angiotensin system that is antifibrotic and anti-inflammatory. In preclinical models, we found that chronic exposure to cigarette smoke, a risk factor for both COPD and IPF and potentially for SARS-CoV-2 infection, significantly increased pulmonary ACE2 protein expression. Further studies are needed to understand the functional implications of ACE2 on lung fibroblasts, a cell type that thus far has received relatively little attention in the context of COVID-19.
新型冠状病毒病与严重肺炎和急性呼吸窘迫综合征相关，可导致易感个体死亡。对于那些康复的患者，新冠病毒后并发症可能包括肺纤维化的发展。导致疾病严重程度或并发症发展的因素尚不清楚。通过使用计算分析和实验数据，我们报告特发性肺纤维化 (IPF) 和慢性阻塞性肺疾病 (COPD) 衍生的肺成纤维细胞表达更高水平的血管紧张素转换酶 2 (ACE2)，这是 SARS-CoV-2 进入的受体，也是肾素-血管紧张素系统的一部分，具有抗纤维化和抗炎作用。在临床前模型中，我们发现慢性暴露于香烟烟雾（COPD 和 IPF 的风险因素，也可能是 SARS-CoV-2 感染的风险因素）显著增加了肺 ACE2 蛋白表达。需要进一步研究以了解 ACE2 对肺成纤维细胞的功能意义，到目前为止，肺成纤维细胞在新冠病毒的背景下相对较少受到关注。
