Corpus overview


MeSH Disease

Human Phenotype

Colitis (2)

Pneumonia (1)



There are no seroprevalence terms in the subcorpus

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    The role of nicotinic receptors in SARS-CoV-2 receptor ACE2 expression in intestinal epithelia

    Authors: Anne Sophie ten Hove; David Jan Brinkman; Andrew Y.F. Li Yim; Caroline Verseijden; Theo B.M. Hakvoort; Iris Admiraal; Olaf Welting; Patricia H.P. van Hamersveld; Valerie Sinniger; Bruno Bonaz; Misha D. Luyer; Wouter J. de Jonge

    doi:10.21203/ Date: 2020-07-21 Source: ResearchSquare

    Background – Recent evidence demonstrated that severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) propagates in intestinal epithelial cells expressing Angiotensin-Converting Enzyme 2 (ACE2), implying that these cells represent an important entry site for the viral infection MESHD. Nicotinic receptors (nAChRs) have been put forward as potential regulators of inflammation MESHD and of ACE2 expression. As vagus nerve stimulation (VNS) activates nAChRs, we aimed to investigate whether VNS can be instrumental in affecting intestinal epithelial ACE2 expression. Methods – By using publicly available datasets we qualified epithelial ACE2 expression in human intestine, and assessed gene co-expression of ACE2 and SARS-CoV-2 priming Transmembrane Serine Protease 2 (TMPRSS2) with nAChRs in intestinal epithelial cells. Next, we investigated mouse and human ACE2 expression in intestinal tissues after chronic VNS via implanted devices. Results – We show co-expression of ACE2 and TMPRSS2 with nAChRs and α7 nAChR in particular in intestinal stem cells, goblet cells, and enterocytes. However, VNS did not affect ACE2 expression in murine or human intestinal tissue, albeit in colitis MESHD colitis HP setting. Conclusions – ACE2 and TMPRSS2 are specifically expressed in epithelial cells of human intestine, and both are co-expressed with nAChRs. However, no evidence for regulation of ACE2 expression through VNS could be found. Hence, there is no indication for a therapeutic value of VNS with respect to SARS-CoV-2 infection MESHD infection risk TRANS infection risk TRANS risk through ACE2 receptors in intestinal epithelia.

    ACE2 expression by colonic epithelial cells is associated with viral infection MESHD, immunity and energy metabolism

    Authors: Jun Wang; Shanmeizi Zhao; Ming Liu; Zhiyao Zhao; Yiping Xu; Ping Wang; Meng Lin; Yanhui Xu; Bing Huang; Xiaoyu Zuo; Zhanghua Chen; Fan Bai; Jun Cui; Andrew M Lew; Jincun Zhao; Yan Zhang; Haibin Luo; Yuxia Zhang

    doi:10.1101/2020.02.05.20020545 Date: 2020-02-07 Source: medRxiv

    Respiratory disease MESHD caused by the 2019 novel coronavirus (2019-nCoV) pneumonia MESHD pneumonia HP first emerged in Wuhan, Hubei Province, China, in December 2019 and spread rapidly to other provinces and other countries. Angiotensin-converting enzyme 2 (ACE2) is the receptor for SARS-CoV and has been suggested to be also the receptor for 2019-nCoV. Paradoxically, ACE2 expression in the lung protects mice from SARS-CoV spike protein induced lung injury MESHD by attenuating the renin-angiotensin system. In the intestine, ACE2 also suppresses intestinal inflammation MESHD by maintaining amino acid homeostasis, antimicrobial peptide expression and ecology of the gut microbiome. Upon analysis of single cell-RNA sequencing data from control subjects and those with colitis MESHD colitis HP or inflammatory bowel disease MESHD (IBD), we found that ACE2 expression in the colonocytes was positively associated with genes regulating viral infection MESHD, innate and cellular immunity, but was negatively associated with viral transcription, protein translation, humoral immunity, phagocytosis and complement activation. In summary, we suggest that ACE2 may play dual roles in mediating the susceptibility and immunity of 2019-nCoV infection MESHD.

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MeSH Disease
Human Phenotype

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