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Molecules. 2022 Jan 27;27(3):862. doi: 10.3390/molecules27030862.
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SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway.SARS-CoV-2 刺突蛋白通过 TLR2 依赖性激活 NF-κB 途径诱导炎症反应。
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The Unique Impact of COVID-19 on Human Gut Microbiome Research.新冠病毒对人类肠道微生物组研究的独特影响。
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Slc26a3 (DRA) in the Gut: Expression, Function, Regulation, Role in Infectious Diarrhea and Inflammatory Bowel Disease.Slc26a3(DRA)在肠道中的表达、功能、调控及其在感染性腹泻和炎症性肠病中的作用。
Inflamm Bowel Dis. 2021 Mar 15;27(4):575-584. doi: 10.1093/ibd/izaa256.
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The role of furin cleavage site in SARS-CoV-2 spike protein-mediated membrane fusion in the presence or absence of trypsin.弗林蛋白酶切割位点在有或无胰蛋白酶存在的情况下,在SARS-CoV-2刺突蛋白介导的膜融合中的作用。
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SARS-CoV-2 strategically mimics proteolytic activation of human ENaC.SARS-CoV-2 策略性地模拟人类 ENaC 的蛋白水解激活。
Elife. 2020 May 26;9:e58603. doi: 10.7554/eLife.58603.
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Diarrhea During COVID-19 Infection: Pathogenesis, Epidemiology, Prevention, and Management.新冠病毒感染期间的腹泻:发病机制、流行病学、预防和管理。
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在 COVID-19 相关腹泻中,肠道转运是否出现功能障碍?

Is intestinal transport dysfunctional in COVID-19-related diarrhea?

机构信息

Leeds Institute for Medical Research at St. James's, St. James's University Hospital, Leeds, United Kingdom.

Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, United Kingdom.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2023 May 1;324(5):G415-G418. doi: 10.1152/ajpgi.00021.2023. Epub 2023 Mar 28.

DOI:10.1152/ajpgi.00021.2023
PMID:36976797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10281778/
Abstract

Diarrhea, often severe, is a recognized and frequently early symptom during acute COVID-19 infection and may persist or develop for the first time in patients with long-COVID, with socioeconomic consequences. Diarrheal mechanisms in these cases are poorly understood. There is evidence for disruption of intestinal epithelial barrier function and also for changes in the gut microbiome, which is critical for gut immunity and metabolism. Whether the SARS-CoV-2 virus has adverse effects on intestinal transport proteins is unclear. However, the ability of the virus to inhibit expression and activity of an aldosterone-regulated epithelial sodium (Na) channel (ENaC) present in human distal colon, which is responsible for Na and water salvage, points to possible disruption of other intestinal transport proteins during COVID-19 infection. In this Perspective, we develop this idea by highlighting possible intestinal transport protein targets for the SARS-CoV-2 virus and discussing how their interactions might be explored in the laboratory.

摘要

腹泻,常为严重,是急性 COVID-19 感染时公认的、常出现的早期症状,且可能在长新冠患者中持续存在或首次出现,并带来社会经济后果。在这些病例中,腹泻的发病机制尚不清楚。有证据表明肠道上皮屏障功能紊乱,以及肠道微生物组发生变化,而肠道微生物组对于肠道免疫和代谢至关重要。SARS-CoV-2 病毒是否对肠道转运蛋白有不良影响尚不清楚。然而,该病毒抑制人远端结肠中存在的醛固酮调节的上皮钠(Na)通道(ENaC)的表达和活性的能力,而 ENaC 负责 Na 和水的重吸收,这表明 COVID-19 感染期间可能会破坏其他肠道转运蛋白。在本观点中,我们通过强调 SARS-CoV-2 病毒可能的肠道转运蛋白靶点,并讨论如何在实验室中探索它们的相互作用,进一步阐述了这一观点。