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肠道微生物及其代谢产物在痛风性关节炎发病机制中的双重调节作用:促进与抑制之间的平衡

The dual regulatory effects of intestinal microorganisms and their metabolites in gouty arthritis pathogenesis: a balance between promotion and inhibition.

作者信息

Qi Peng, Li Longcan, Zhang Jianrong, Ren Ling, Xie Xingwen

机构信息

Gansu University of Traditional Chinese Medicine, Lanzhou, China.

Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou, China.

出版信息

Front Immunol. 2025 Jun 18;16:1591369. doi: 10.3389/fimmu.2025.1591369. eCollection 2025.


DOI:10.3389/fimmu.2025.1591369
PMID:40607437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12213782/
Abstract

Gout is an arthritis characterized by the deposition of urate crystals, often accompanied by robust inflammatory responses. The gut microbiome profoundly influences gout pathogenesis, progression, and management by affecting uric acid metabolism, immune responses, and intestinal barrier function. Studies reveal that gut microorganisms exert a dual role in gout development. Gout patients typically exhibit increased harmful bacterial abundance and reduced beneficial species. Harmful bacteria and associated metabolites can influence systemic uric acid levels by regulating excretion and synthesis, thereby promoting gout manifestations. Conversely, beneficial bacteria interact with the host immune system to inhibit inflammation and modulate the inflammatory state of joints. Furthermore, the gut microbiome can significantly impact gout treatment efficacy through its influence on drug metabolism and absorption. Research highlighting the gut-joint-inflammation axis offers novel therapeutic strategies for gout, suggesting that future approaches may involve microbiome modulation to enhance clinical outcomes.

摘要

痛风是一种以尿酸盐结晶沉积为特征的关节炎,常伴有强烈的炎症反应。肠道微生物群通过影响尿酸代谢、免疫反应和肠道屏障功能,对痛风的发病机制、进展和管理产生深远影响。研究表明,肠道微生物在痛风发展中发挥双重作用。痛风患者通常表现出有害细菌丰度增加和有益菌种类减少。有害细菌及其相关代谢产物可通过调节排泄和合成来影响全身尿酸水平,从而促进痛风表现。相反,有益菌与宿主免疫系统相互作用以抑制炎症并调节关节的炎症状态。此外,肠道微生物群可通过影响药物代谢和吸收,显著影响痛风治疗效果。强调肠道-关节-炎症轴的研究为痛风提供了新的治疗策略,表明未来的方法可能涉及调节微生物群以改善临床结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/e6eabd9ae4a3/fimmu-16-1591369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/926c50935831/fimmu-16-1591369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/6c3ca020098f/fimmu-16-1591369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/e6eabd9ae4a3/fimmu-16-1591369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/926c50935831/fimmu-16-1591369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/6c3ca020098f/fimmu-16-1591369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f035/12213782/e6eabd9ae4a3/fimmu-16-1591369-g003.jpg

相似文献

[1]
The dual regulatory effects of intestinal microorganisms and their metabolites in gouty arthritis pathogenesis: a balance between promotion and inhibition.

Front Immunol. 2025-6-18

[2]
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[7]
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[8]
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[10]
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本文引用的文献

[1]
Leveraging real-world data to advance biomarker discovery and precision oncology.

Cancer Cell. 2025-4-14

[2]
Computational methods and biomarker discovery strategies for spatial proteomics: a review in immuno-oncology.

Brief Bioinform. 2024-7-25

[3]
Study on the effects of intestinal flora on gouty arthritis.

Front Cell Infect Microbiol. 2024

[4]
Commentary: Gut microbiota reduce the risk of hyperuricemia and gout in the human body.

Acta Pharm Sin B. 2024-1

[5]
A widely distributed gene cluster compensates for uricase loss in hominids.

Cell. 2023-8-3

[6]
Sinomenine ameliorates rheumatoid arthritis by modulating tryptophan metabolism and activating aryl hydrocarbon receptor via gut microbiota regulation.

Sci Bull (Beijing). 2023-7-30

[7]
Relationship between gut microbiota and rheumatoid arthritis: A bibliometric analysis.

Front Immunol. 2023

[8]
Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritis multiple pathways.

Front Cell Infect Microbiol. 2023

[9]
Gut commensal alleviates inflammatory arthritis.

Gut. 2023-9

[10]
The role of gut microbiota in gout: Is gut microbiota a potential target for gout treatment.

Front Cell Infect Microbiol. 2022

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