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探讨带状疱疹和带状疱疹后神经痛患者的血液转录组特征。

Exploring blood transcriptomic signatures in patients with herpes zoster and postherpetic neuralgia.

机构信息

Department of Pain Management, Affiliated Hospital of Hebei University/School of Clinical Medicine, Hebei University, Baoding, Hebei, China.

School of Basic Medicine, Hebei University, Baoding, Hebei, China.

出版信息

Front Cell Infect Microbiol. 2024 Aug 15;14:1425393. doi: 10.3389/fcimb.2024.1425393. eCollection 2024.

DOI:10.3389/fcimb.2024.1425393
PMID:39211798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11358128/
Abstract

Postherpetic neuralgia (PHN) is a common, severe, and hard-to-treat chronic pain condition in clinics. Although PHN is developed from herpes zoster (HZ), the developing mechanism is unknown. A previous study investigated blood metabolomic and proteomic profiling in patients with PHN and HZ. The current study aims to explore the blood transcriptomic signature of PHN compared to HZ patients. Whole blood from eight PHN and 15 HZ patients was used for RNA-Seq analysis. There were 82 and 1,788 genes detected specifically in the PHN and HZ groups, respectively. PHN-specific genes are involved in viral infection, lipid and carbohydrate metabolism, and immune response. For genes coexpressed in PHN and HZ patients, there were 407 differential expression genes (DEGs), including 205 upregulated (UP DEGs) and 202 downregulated (DOWN DEGs) in PHN compared to HZ groups. DEGs are involved in viral infection, type I interferon (IFN), and hemoglobin and oxygen carrier activity. UP DEGs are associated with regulatory T cells (Tregs), activated NK cells, and neutrophils, while DOWN DEGs are associated with Tregs, resting NK cells, and monocytes. The results suggest that the metabolism of lipid, glycan, and nucleotides, type I IFN signaling, and altered neutrophil activation are associated with and might contribute to the development of PHN in HZ. It is also suggested that persistent or altered activation of nonspecific immunity may contribute to the development of PHN from HZ.

摘要

带状疱疹后神经痛(PHN)是临床常见的严重且难以治疗的慢性疼痛病症。虽然 PHN 由带状疱疹(HZ)发展而来,但发病机制尚不清楚。先前的研究调查了 PHN 患者和 HZ 患者的血液代谢组学和蛋白质组学特征。本研究旨在探索与 HZ 患者相比,PHN 的血液转录组特征。从 8 名 PHN 和 15 名 HZ 患者中采集全血进行 RNA-Seq 分析。PHN 组和 HZ 组分别特异性检测到 82 个和 1788 个基因。PHN 特异性基因参与病毒感染、脂质和碳水化合物代谢以及免疫反应。在 PHN 和 HZ 患者共表达的基因中,有 407 个差异表达基因(DEGs),与 HZ 相比,PHN 组有 205 个上调(UP DEGs)和 202 个下调(DOWN DEGs)。DEGs 参与病毒感染、I 型干扰素(IFN)和血红蛋白及氧载体活性。UP DEGs 与调节性 T 细胞(Tregs)、活化 NK 细胞和中性粒细胞相关,而 DOWN DEGs 与 Tregs、静息 NK 细胞和单核细胞相关。结果表明,脂质、聚糖和核苷酸代谢、I 型 IFN 信号转导以及中性粒细胞激活的改变与 HZ 中 PHN 的发生发展有关,并可能与之相关。此外,非特异性免疫的持续或改变的激活也可能导致 HZ 向 PHN 的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/4e5d2be8bd13/fcimb-14-1425393-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/4e5d2be8bd13/fcimb-14-1425393-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/a45d7eea3ec7/fcimb-14-1425393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/4d2775a52de4/fcimb-14-1425393-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/b5ad6db35f08/fcimb-14-1425393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/fc9c84f704dc/fcimb-14-1425393-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc62/11358128/ba32a5180f7c/fcimb-14-1425393-g007.jpg
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