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采用胶原诱导性关节炎模型和胶原抗体诱导性关节炎模型对类风湿关节炎发病机制的新研究:涉及细菌菌群的新见解

New Studies of Pathogenesis of Rheumatoid Arthritis with Collagen-Induced and Collagen Antibody-Induced Arthritis Models: New Insight Involving Bacteria Flora.

作者信息

Hashida Ryoichi, Shimozuru Yasunori, Chang Jessica, Agosto-Marlin Ibis, Waritani Takaki, Terato Kuniaki

机构信息

Chondrex Inc., 16928 Woodinville-Redmond Rd NE STE B101, Woodinville, WA 98072, USA.

出版信息

Autoimmune Dis. 2021 Mar 25;2021:7385106. doi: 10.1155/2021/7385106. eCollection 2021.

DOI:10.1155/2021/7385106
PMID:33833871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8016593/
Abstract

Much public research suggests that autoimmune diseases such as rheumatoid arthritis (RA) are induced by aberrant "self" immune responses attacking autologous tissues and organ components. However, recent studies have reported that autoimmune diseases may be triggered by dysbiotic composition changes of the intestinal bacteria and an imbalance between these bacteria and intestinal immune systems. However, there are a few solid concepts or methods to study the putative involvement and relationship of these inner environmental factors in RA pathogenesis. Fortunately, Collagen-Induced Arthritis (CIA) and Collagen Antibody-Induced Arthritis (CAIA) models have been widely used as animal models for studying the pathogenesis of RA. In addition to RA, these models can be extensively used as animal models for studying complicated hypotheses in many diseases. In this review, we introduce some basic information about the CIA and CAIA models as well as how to apply these models effectively to investigate relationships between the pathogenesis of autoimmune diseases, especially RA, and the dysbiosis of intestinal bacterial flora.

摘要

许多公共研究表明,类风湿性关节炎(RA)等自身免疫性疾病是由异常的“自身”免疫反应攻击自体组织和器官成分所致。然而,最近的研究报告称,自身免疫性疾病可能由肠道细菌的生态失调组成变化以及这些细菌与肠道免疫系统之间的失衡引发。然而,目前几乎没有坚实的概念或方法来研究这些内在环境因素在类风湿性关节炎发病机制中的假定参与情况及其关系。幸运的是,胶原诱导性关节炎(CIA)和胶原抗体诱导性关节炎(CAIA)模型已被广泛用作研究类风湿性关节炎发病机制的动物模型。除了类风湿性关节炎外,这些模型还可广泛用作研究许多疾病复杂假说的动物模型。在本综述中,我们介绍了一些关于CIA和CAIA模型的基本信息,以及如何有效应用这些模型来研究自身免疫性疾病,尤其是类风湿性关节炎的发病机制与肠道菌群失调之间的关系。

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New Studies of Pathogenesis of Rheumatoid Arthritis with Collagen-Induced and Collagen Antibody-Induced Arthritis Models: New Insight Involving Bacteria Flora.采用胶原诱导性关节炎模型和胶原抗体诱导性关节炎模型对类风湿关节炎发病机制的新研究:涉及细菌菌群的新见解
Autoimmune Dis. 2021 Mar 25;2021:7385106. doi: 10.1155/2021/7385106. eCollection 2021.
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Collagen antibody induced arthritis.胶原抗体诱导的关节炎
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本文引用的文献

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Metagenome-wide association study of gut microbiome revealed novel aetiology of rheumatoid arthritis in the Japanese population.基于宏基因组关联研究的日本人群肠道微生物组分析揭示类风湿关节炎的新病因。
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Heat-killed probiotic regulates the body's regulatory immunity to attenuate subsequent experimental autoimmune arthritis.热灭活益生菌调节机体的调节性免疫,从而减轻随后的实验性自身免疫性关节炎。
Immunol Lett. 2019 Dec;216:89-96. doi: 10.1016/j.imlet.2019.10.009. Epub 2019 Oct 20.
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Analysis of intestinal immunity and flora in a collagen-induced mouse arthritis model: differences during arthritis progression.
Emodin alleviates arthritis pain through reducing spinal inflammation and oxidative stress.
大黄素通过减轻脊髓炎症和氧化应激缓解关节炎疼痛。
Mol Pain. 2022 Apr;18:17448069221146398. doi: 10.1177/17448069221146398.
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Active rheumatoid arthritis in a mouse model is not an independent risk factor for periprosthetic joint infection.在小鼠模型中,活动性类风湿关节炎不是假体周围关节感染的独立危险因素。
PLoS One. 2021 Aug 16;16(8):e0250910. doi: 10.1371/journal.pone.0250910. eCollection 2021.
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4
Drug-microbiota interactions and treatment response: Relevance to rheumatoid arthritis.药物-微生物群相互作用与治疗反应:与类风湿关节炎的相关性
AIMS Microbiol. 2018 Oct 26;4(4):642-654. doi: 10.3934/microbiol.2018.4.642. eCollection 2018.
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Cancer immunotherapy with check point inhibitor can cause autoimmune adverse events due to loss of Treg homeostasis.癌症免疫疗法中的检查点抑制剂可能会由于 Treg 稳态的丧失而导致自身免疫性不良反应。
Semin Cancer Biol. 2020 Aug;64:29-35. doi: 10.1016/j.semcancer.2019.01.006. Epub 2019 Feb 1.
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Microbiota-Dependent Involvement of Th17 Cells in Murine Models of Inflammatory Arthritis.肠道菌群依赖的 Th17 细胞在炎症性关节炎的小鼠模型中的作用
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Probiotic Species in the Modulation of Gut Microbiota: An Overview.益生菌物种对肠道微生物群的调节:概述。
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