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利用生物信息学和系统生物学发现结节病和新冠肺炎之间的共同致病过程。

Using bioinformatics and systems biology to discover common pathogenetic processes between sarcoidosis and COVID-19.

作者信息

Fu Lanyi, Yao Maolin, Liu Xuedong, Zheng Dong

机构信息

Laboratory of Genetics and Molecular Biology, College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, China.

出版信息

Gene Rep. 2022 Jun;27:101597. doi: 10.1016/j.genrep.2022.101597. Epub 2022 Mar 18.

DOI:10.1016/j.genrep.2022.101597
PMID:35317263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8931993/
Abstract

The coronavirus disease (COVID-19) pandemic caused by SARS-CoV-2 is ongoing. Individuals with sarcoidosis tend to develop severe COVID-19; however, the underlying pathological mechanisms remain elusive. To determine common transcriptional signatures and pathways between sarcoidosis and COVID-19, we investigated the whole-genome transcriptome of peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 and sarcoidosis and conducted bioinformatic analysis, including gene ontology and pathway enrichment, protein-protein interaction (PPI) network, and gene regulatory network (GRN) construction. We identified 33 abnormally expressed genes that were common between COVID-19 and sarcoidosis. Functional enrichment analysis showed that these differentially expressed genes were associated with cytokine production involved in the immune response and T cell cytokine production. We identified several hub genes from the PPI network encoded by the common genes. These hub genes have high diagnostic potential for COVID-19 and sarcoidosis and can be potential biomarkers. Moreover, GRN analysis identified important microRNAs and transcription factors that regulate the common genes. This study provides a novel characterization of the transcriptional signatures and biological processes commonly dysregulated in sarcoidosis and COVID-19 and identified several critical regulators and biomarkers. This study highlights a potential pathological association between COVID-19 and sarcoidosis, establishing a theoretical basis for future clinical trials.

摘要

由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的冠状病毒病(COVID-19)大流行仍在持续。结节病患者往往会发展为重症COVID-19;然而,其潜在的病理机制仍不清楚。为了确定结节病和COVID-19之间共同的转录特征和途径,我们研究了COVID-19患者和结节病患者外周血单个核细胞(PBMC)的全基因组转录组,并进行了生物信息学分析,包括基因本体论和途径富集、蛋白质-蛋白质相互作用(PPI)网络以及基因调控网络(GRN)构建。我们鉴定出33个在COVID-19和结节病之间共同异常表达的基因。功能富集分析表明,这些差异表达基因与免疫反应中涉及的细胞因子产生以及T细胞细胞因子产生有关。我们从共同基因编码的PPI网络中鉴定出几个枢纽基因。这些枢纽基因对COVID-19和结节病具有较高的诊断潜力,可能成为潜在的生物标志物。此外,GRN分析确定了调控共同基因的重要微小RNA和转录因子。本研究提供了结节病和COVID-19中共同失调的转录特征和生物学过程的新特征,并鉴定出几个关键调节因子和生物标志物。本研究突出了COVID-19与结节病之间潜在的病理关联,为未来的临床试验奠定了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/962ec9b91e65/gr5_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/2aec3096f456/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/5449e258f34c/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/a677404e090b/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/67f3087cb78c/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/962ec9b91e65/gr5_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/2aec3096f456/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/5449e258f34c/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/a677404e090b/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/67f3087cb78c/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dae6/8931993/962ec9b91e65/gr5_lrg.jpg

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