Upregulation of TNF-α and IL-6 in palindromic rheumatism: A biomarker link to rheumatoid arthritis progression and therapeutic implications

IF 1 Q4 GENETICS & HEREDITY

Gene Reports Pub Date : 2025-02-19 DOI:10.1016/j.genrep.2025.102175

Kamran Javidi-Aghdam , Mostafa Akbarzadeh-Khiavi , Sepideh Parvizpour , Shima Rahmani , Faranak Sheikhmonazzah , Ata Khodaparast , Aida Malek Mahdavi , Azam Safary , Alireza Khabbazi

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引用次数: 0

Abstract

Background

Palindromic rheumatism (PR) is a rare autoimmune disease characterized by episodic joint inflammation, often progressing to rheumatoid arthritis (RA). However, the molecular mechanisms driving this transition remain unclear. This study aimed to investigate the roles of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the PR progression toward RA by examining their serum levels and gene expression in patients with PR and RA, compared to healthy controls (HCs).

Methods

This cross-sectional study was conducted on peripheral blood mononuclear cells (PBMCs) obtained from patients with PR (n = 17), RA (n = 35), and age-sex-matched HCs (n = 38). TNF-α and IL-6 serum levels were quantified using enzyme-linked immunosorbent assay, and mRNA levels were analyzed through real-time PCR. Classification and regression tree (CART) models were employed to determine the relevance of these cytokines in RA.

Results

TNF-α serum levels in PR, RA, and HCs were measured at 10.5 ± 1.3, 8.9 ± 1.1, and 6.3 ± 0.8 pg/mL, respectively. IL-6 levels were 6.84 ± 2.6, 6.65 ± 2.5, and 1.10 ± 0.5 pg/mL for the same groups. Both cytokines were significantly elevated in PR and RA patients compared to HCs (p < 0.05). Gene expression analysis confirmed the upregulation of TNF-α and IL-6 in both the PR and RA groups.

Conclusions

These findings suggest that the upregulation of TNF-α and IL-6 may be key factors driving the progression of PR to RA. Targeting these cytokines could represent a novel therapeutic strategy to prevent disease advancement.

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复发性风湿病中TNF-α和IL-6的上调：与类风湿关节炎进展和治疗意义相关的生物标志物

背景：复发性风湿病（PR）是一种罕见的自身免疫性疾病，以间歇性关节炎症为特征，常进展为类风湿关节炎（RA）。然而，驱动这种转变的分子机制仍不清楚。本研究旨在通过检测PR和RA患者血清中肿瘤坏死因子-α (TNF-α)和白细胞介素-6 （IL-6）的水平和基因表达，与健康对照组（hc）相比，探讨肿瘤坏死因子-α和白细胞介素-6在PR向RA进展中的作用。方法采用横断面研究方法，对PR （n = 17）、RA （n = 35）和年龄性别匹配的hc （n = 38）患者外周血单个核细胞（PBMCs）进行研究。采用酶联免疫吸附法定量血清TNF-α和IL-6水平，real-time PCR分析mRNA水平。采用分类和回归树（CART）模型来确定这些细胞因子在RA中的相关性。结果PR、RA、hc组血清stnf -α水平分别为10.5±1.3、8.9±1.1、6.3±0.8 pg/mL。各组IL-6水平分别为6.84±2.6、6.65±2.5、1.10±0.5 pg/mL。与hcc患者相比，PR和RA患者两种细胞因子均显著升高(p <；0.05)。基因表达分析证实了PR组和RA组TNF-α和IL-6的上调。结论TNF-α和IL-6的上调可能是PR向RA发展的关键因素。靶向这些细胞因子可能代表一种新的治疗策略，以防止疾病的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.