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 is not known. Using computational analysis with experimental data, we report that IPF and COPD-derived lung fibroblasts express higher levels of ACE2, the receptor for SARS-CoV-2 entry and part of the renin-angiotensin system that is anti-fibrotic 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 as received relatively little attention in the context of COVID-19.

中文翻译：

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血管紧张素转换酶2（ACE2）在COPD和IPF成纤维细胞中的表达-COVID-19中被遗忘的细胞

COVID-19大流行与严重的肺炎和急性呼吸窘迫综合征相关，导致易感人群死亡。对于那些康复的患者，COVID-19后的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。使用具有实验数据的计算分析，我们报告IPF和COPD衍生的肺成纤维细胞表达更高水平的ACE2，SARS-CoV-2进入的受体以及部分抗纤维化和抗炎的肾素-血管紧张素系统。在临床前模型中，我们发现长期接触香烟烟雾是COPD和IPF的危险因素，也可能是SARS-CoV-2感染的危险因素，可显着增加肺ACE2蛋白的表达。