Intestinal Inflammation Modulates the Expression of ACE2 and TMPRSS2 and Potentially Overlaps With the Pathogenesis of SARS-CoV-2-related Disease.
Intestinal Inflammation Modulates the Expression of ACE2 and TMPRSS2 and Potentially Overlaps With the Pathogenesis of SARS-CoV-2-related Disease.
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DOI：
10.1053/j.gastro.2020.09.029
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发表时间：
2021-01
期刊：
影响因子：
29.4
通讯作者：
Mehandru S
中科院分区：
文献类型：
--
作者：
Suárez-Fariñas M;Tokuyama M;Wei G;Huang R;Livanos A;Jha D;Levescot A;Irizar H;Kosoy R;Cording S;Wang W;Losic B;Ungaro RC;Di'Narzo A;Martinez-Delgado G;Suprun M;Corley MJ;Stojmirovic A;Houten SM;Peters L;Curran M;Brodmerkel C;Perrigoue J;Friedman JR;Hao K;Schadt EE;Zhu J;Ko HM;Cho J;Dubinsky MC;Sands BE;Ndhlovu L;Cerf-Bensusan N;Kasarskis A;Colombel JF;Harpaz N;Argmann C;Mehandru S
胃肠道症状和粪便中高水平的病毒RNA表明，严重急性呼吸综合征冠状病毒2(SARS-CoV-2)在肠道细胞内复制活跃。在这里，在多个大型炎症性肠病患者队列中，我们研究了冠状病毒病2019(新冠肺炎)、肠道炎症和炎症性肠病治疗之间的交叉。小肠上皮细胞刷状缘处ACE2的显著表达支持SARS-CoV-2的肠道感染性。常用的IBD药物，无论是生物的还是非生物的，都不会显著影响未发炎的肠道中ACE2和TMPRSS2受体的表达。此外，我们定义了对新冠肺炎感染的分子反应，这些反应也在炎症性肠病中丰富，指出新冠肺炎和炎症性肠病之间存在共同的分子网络。这些数据使人们对新冠肺炎和炎症性肠病相关炎症的融合有了新的认识，并提供了支持进一步研究治疗新冠肺炎的特定炎症性肠病药物的机械性见解。预印DOI：https://doi.org/10.1101/2020.05.21.109124
The presence of gastrointestinal symptoms and high levels of viral RNA in the stool suggest active severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication within enterocytes. Here, in multiple, large cohorts of patients with inflammatory bowel disease (IBD), we have studied the intersections between Coronavirus Disease 2019 (COVID-19), intestinal inflammation, and IBD treatment. A striking expression of ACE2 on the small bowel enterocyte brush border supports intestinal infectivity by SARS-CoV-2. Commonly used IBD medications, both biologic and nonbiologic, do not significantly impact ACE2 and TMPRSS2 receptor expression in the uninflamed intestines. In addition, we have defined molecular responses to COVID-19 infection that are also enriched in IBD, pointing to shared molecular networks between COVID-19 and IBD. These data generate a novel appreciation of the confluence of COVID-19– and IBD-associated inflammation and provide mechanistic insights supporting further investigation of specific IBD drugs in the treatment of COVID-19. Preprint doi: https://doi.org/10.1101/2020.05.21.109124
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