Background: The mechanism for the association between traffic-derived particulate matter less than 10 microns (PM10) and cases of COVID-19 disease reported in epidemiological studies is unknown. To infect cells, the spike protein of SARS-CoV-2 interacts with angiotensin-converting enzyme 2 (ACE2) on host airway cells. Increased ACE2 expression in lower airway cells in active smokers, suggests a potential mechanism whereby PM10 increases vulnerability to COVID-19 disease. Objective: To assess the effect of traffic-derived PM10 on human airway epithelial cell ACE2 expression in vitro. Methods: PM10 was collected from Marylebone Road (London) using a kerbside impactor. A549 and human primary nasal epithelial cells were cultured with PM10 for 2 h, and ACE2 expression (median fluorescent intensity; MFI) assessed by flow cytometry. We included cigarette smoke extract as a putative positive control. Data were analysed by either Mann-Whitney test, or Kruskal-Wallis with multiple comparisons test. Results: PM10 at 10 μg/mL, and 20 μg/mL increased ACE2 expression in A549 cells (P<0.05, 0.01 vs. medium control, respectively). Experiments using a single PM10 concentration (10 μg/mL), found increased ACE2 expression in both A549 cells (control vs. PM10, median (IQR) MFI; 470 (0.1 to 1114) vs 6217 (5071 to 8506), P<0.01), and in human primary epithelial cells (0 (0 to 591) vs. 4000 (2610 to 7853), P<0.05). Culture of A549 cells with 5% cigarette smoke extract increased ACE2 expression (n=4, 0 (0 to 28) vs. 9088 (7557 to 15831, P<0.05). Conclusion: Traffic-related PM10 increases the expression of the receptor for SARS-CoV-2 in human respiratory epithelial cells.

中文翻译：

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人源气道上皮细胞中交通源性颗粒物和血管紧张素转换酶2的表达

背景：在流行病学研究中，小于10微米的交通源性颗粒物（PM10）与COVID-19疾病病例之间的关联机制尚不清楚。为了感染细胞，SARS-CoV-2的突触蛋白与宿主气道细胞上的血管紧张素转换酶2（ACE2）相互作用。活跃吸烟者下呼吸道细胞中ACE2表达的增加，提示了PM10增加对COVID-19疾病的易感性的潜在机制。目的：探讨交通源性PM10对人气道上皮细胞ACE2表达的影响。方法：使用路边撞击器从马里波恩路（伦敦）收集PM10。将A549和人原发性鼻上皮细胞与PM10培养2小时，并通过流式细胞仪评估ACE2表达（中值荧光强度； MFI）。我们将香烟烟雾提取物作为推定的阳性对照。通过Mann-Whitney检验或Kruskal-Wallis进行多重比较检验来分析数据。结果：10μg/ mL和20μg/ mL的PM10可以增加A549细胞中ACE2的表达（相对于中度对照，分别为P <0.05，0.01）。使用单一PM10浓度（10μg/ mL）进行的实验发现，两个A549细胞中ACE2表达均增加（对照vs. PM10，中位数（IQR）MFI； 470（0.1至1114）与6217（5071至8506），P <0.01 ），以及人类原代上皮细胞（0（0至591）与4000（2610至7853），P <0.05）。用5％香烟烟雾提取物培养A549细胞可提高ACE2的表达（n = 4，0（0至28），而9088（7557至15831，P <0.05）。结论：交通相关的PM10可增加ACE2受体的表达。人呼吸道上皮细胞中的SARS-CoV-2。