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新冠病毒疾病(COVID-19)患者肠道共生菌的改变

Alterations of the gut commensal in patients with COVID-19.

作者信息

Dai Zhi-Ming, Xu Meng-Lu, Zhang Qing-Qing, Zhu Bo, Wu Jun-Zhe, Liu Qi, Li Ying, Li Hong-Bao

机构信息

Department of Anesthesiology, The First People's Hospital of Xianyang, Xianyang, China.

Department of Nephrology, The First Affiliated Hospital of Xi'an Medical University, Xi'an, China.

出版信息

Virulence. 2025 Dec;16(1):2505999. doi: 10.1080/21505594.2025.2505999. Epub 2025 May 18.

DOI:10.1080/21505594.2025.2505999
PMID:40360188
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12091934/
Abstract

Dysbiosis of gut microbiota is well established in coronavirus disease 2019 (COVID-19). While studies have attempted to establish a link between the gut commensal () and COVID-19, the findings have been inconsistent and sometimes controversial. The intestinal microbial abundance information of COVID-19 patients was acquired and analysed from GMrepo database. Subsequently, metabolites, target-genes, and metabolite-target relationships was extracted from GutMGene database. Lastly, coronascape module in Metascape database is used for gene annotation and enrichment analysis in various host cells and tissues after SARS-CoV-2 infection. The results indicated that, in comparison to healthy people, was significantly elevated in COVID-19 patients. This bacterium was found to be associated with heightened expression of IL-10, TLR2, TLR4, CLGN, CLDN4, TJP2, and TJP3, while concurrently experiencing a reduction in the expression of IL-12A and IL-12B in humans. The regulatory genes of primarily enhance responses to viruses and cytokines, positively regulate cell migration, and control epithelial cell proliferation. Our study revealed a significant increase in the gut commensal in COVID-19 patients. This bacterium can modulate host immune responses and may also serve as a probiotic with antiviral properties.

摘要

肠道微生物群失调在2019冠状病毒病(COVID-19)中已得到充分证实。虽然已有研究试图建立肠道共生菌与COVID-19之间的联系,但其结果并不一致,有时还存在争议。从GMrepo数据库中获取并分析了COVID-19患者的肠道微生物丰度信息。随后,从GutMGene数据库中提取了代谢物、靶基因以及代谢物-靶标关系。最后,利用Metascape数据库中的coronascape模块对严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染后各种宿主细胞和组织中的基因进行注释和富集分析。结果表明,与健康人相比,COVID-19患者体内的[某种细菌名称]显著升高。研究发现,这种细菌与人类白细胞介素-10(IL-10)、Toll样受体2(TLR2)、Toll样受体4(TLR4)、claudin相关基因(CLGN)、紧密连接蛋白4(CLDN4)、紧密连接蛋白2(TJP2)和紧密连接蛋白3(TJP3)的表达升高有关,同时白细胞介素-12A(IL-12A)和白细胞介素-12B(IL-12B)的表达降低。[某种细菌名称]的调控基因主要增强对病毒和细胞因子的反应,正向调节细胞迁移,并控制上皮细胞增殖。我们的研究表明,COVID-19患者肠道共生菌[某种细菌名称]显著增加。这种细菌可以调节宿主免疫反应,也可能作为一种具有抗病毒特性的益生菌。 (注:原文中部分细菌名称未给出具体中文,用[某种细菌名称]代替)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/55b89424f76a/KVIR_A_2505999_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/a73673fa0e3a/KVIR_A_2505999_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/e43acb121bfa/KVIR_A_2505999_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/476e6473005c/KVIR_A_2505999_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/55b89424f76a/KVIR_A_2505999_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/a73673fa0e3a/KVIR_A_2505999_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/e43acb121bfa/KVIR_A_2505999_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/476e6473005c/KVIR_A_2505999_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eef6/12091934/55b89424f76a/KVIR_A_2505999_F0004_OC.jpg

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本文引用的文献

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