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Expression of Receptors for SARS-CoV-2 in the Gut of Patients with Inflammatory Bowel Disease

机译：SARS-COV-2在炎症性肠病患者肠道中的受体的表达

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To the Editor: Coronavirus disease 2019 (COVID-19) is a new infectious respiratory disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), one of the seven coronaviruses known to infect humans. Because of the human-to-human transmission route, as of March 25, 2020, 38,0000 subjects have been diagnosed with SARS-CoV-2, and more than 10,000 infected patients have died worldwide. The clinical spectrum of SARS-CoV-2 ranges from asymptomatic or mild respiratory disease to pneumonia with respiratory distress syndrome and/or sepsis, which can result in a fatal outcome. Common symptoms are fever, cough, and shortness of breath, but gastrointestinal symptoms can occur in some patients. 1 SARS-CoV-2 infection is especially frequent in the elderly population and in people with coexisting pathologies and weakened immune systems. The latter could include patients with Crohn’s disease (CD) and patients with ulcerative colitis (UC), the major inflammatory bowel diseases (IBDs) in human beings, as these pathologies are associated with an increased risk of complications, including infections, due to concurrent therapy with immunosuppressive drugs and/or the chronicity of gut inflammation. 2 To gain entry into cells, SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), a protein that is highly expressed in the human intestine. 3 Evaluation of the distribution of the virus in human biological samples revealed that more than half of the fecal samples of patients with COVID-19-driven pneumonia were positive for SARS-CoV-2, and about one-fifth of infected patients remained positive in stools after becoming negative in respiratory samples. 4 These observations suggest that human intestinal tract could serve as an alternative infection route for SARS-CoV-2. If this is true, we could hypothesize that patients with active IBD face an increased risk of SARS-CoV-2 infection, as inflammation can enhance ACE2 expression. We performed a gene array of biopsy samples taken from the inflamed colonic mucosa of six patients with CD, seven patients with UC and six normal controls and initially compared the expression of ACE2 between inflamed and uninflamed samples. Four IBD patients were on mesalazine, three were on steroids and the remaining were off therapy. The study was approved by the local Ethics Committee (protocol number: 154/12). ACE2 abundance was 1.3 times higher in CD and 1.27 times lower in UC, respectively than in the control samples ( Fig. 1 ). Although transmission of SARS-CoV-2 occurs primarily via respiratory droplets, the content of ACE2 is rather low in the lung compared to other human tissues, thus suggesting that SARS-CoV-2 infection also relies on coreceptors and/or other factors expressed by the host. 5 Analysis of these factors in IBD tissues revealed that ANPEP, alanyl aminopeptidase, a host receptor targeted by many viruses belonging to the family Coronaviridae, and DPP4, the receptor for Middle East respiratory syndrome coronavirus, were decreased in UC compared to controls. Moreover, UC samples exhibit decreased expression of the serine protease TMPRSS2, whose activity is crucial in promoting cleavage of the spike (S) protein of the virus, thereby allowing fusion of viral and cellular membranes. 3 In contrast, CD samples exhibited a slight increase in the gene expression of DPP4 and TMPRSS2 and reduced expression of ANPEP compared to controls ( Fig. 1 ). Thus, we can speculate that IBD-associated inflammation by itself does not enhance expression of the factors allowing extrarespiratory transmission of SARS-CoV-2.
机译：向编辑：2019年冠状病毒疾病（Covid-19）是一种新的传染性呼吸道疾病，由严重急性呼吸综合征冠状病毒-2（SARS-COV-2）引起的，其七个冠状病毒是一种感染人类的​​血管吻合器之一。由于人对人类传输路线，截至3月25日，截至3月25日，38,0000名受试者已被诊断为SARS-COV-2，并且超过10,000名受感染的患者在全世界死亡。 SARS-COV-2的临床谱来自无症状或轻度呼吸道疾病与呼吸窘迫综合征和/或败血症的肺炎，这可能导致致命结果。常见的症状是发烧，咳嗽和呼吸急促，但在某些患者中可能发生胃肠道症状。 1 SARS-COV-2感染在老年人人口中特别频繁频繁，并且在共存病理和免疫系统减弱的人中尤其频繁。后者可以包括患有克罗恩病（CD）和溃疡性结肠炎（UC）患者的患者，人类的主要炎症肠疾病（IBDS），因为这些病例与随着并发的影响，包括感染的风险增加治疗免疫抑制药物和/或肠道炎症的慢性。 2为了进入细胞，SARS-COV-2使用血管紧张素转换酶2（ACE2），一种在人肠中高度表达的蛋白质。 3评价人体生物样品中病毒分布显示，患有Covid-19驱动的肺炎患者的超过一半的粪便样本对于SARS-COV-2呈阳性，并且约五分之一的感染患者保持阳性在呼吸样品中变阴性后粪便。 4这些观察结果表明，人类肠道可以作为SARS-COV-2的替代感染途径。如果这是真的，我们可以假设有源IBD的患者面临SARS-COV-2感染的风险增加，因为炎症可以增强ACE2表达。我们进行了一种基因阵列从发炎的粘膜粘膜中患有六名患者的发炎性粘膜粘膜，7名患有UC和六个正常对照的患者，并且最初将ACE2的表达与发炎和未充满的样品之间的表达进行了比较。四个IBD患者在甲烷嗪上，三种是类固醇，其余的脱离治疗。该研究由当地伦理委员会批准（议定书号：154/12）。 ACE2的丰度在CD中的比率为1.3倍，uc分别比对照样品中的1.27倍（图1）。尽管SARS-COV-2的传播主要通过呼吸液滴发生，但与其他人组织相比，肺部含量2的含量相当较低，因此表明SARS-COV-2感染也依赖于承受者和/或所表达的其他因素。主人。 5分析IBD组织中的这些因素显示，与对照组的许多病毒靶向的宿主受体，由属于家庭冠状病毒，中东呼吸综合征冠状病毒的受体靶向的宿主受体在UC中降低。此外，UC样品表现出丝氨酸蛋白酶TMPRSS2的表达降低，其活性在促进病毒的尖峰裂解方面至关重要，从而允许融合病毒和细胞膜。 3相比之下，CD样品表现出DPP4和TMPRS2的基因表达略有增加，与对照相比，ANPEP的表达降低（图1）。因此，我们可以推测IBD相关的炎症本身并不能增强允许SARS-COV-2引起的因素的表达。

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