High fat diet increases the severity of collagen-induced arthritis in mice by altering the gut microbial community.

IF 2 4区医学 Q3 RHEUMATOLOGY

Advances in Rheumatology Pub Date : 2024-05-30 DOI:10.1186/s42358-024-00382-y

Yang Zhang, Jie Zhang, Yantong Liu, Shuang Ren, Ning Tao, Fanyan Meng, Qi Cao, Ruoshi Liu

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引用次数: 0

Abstract

Objectives: Research has demonstrated that obesity may be associated with rheumatoid arthritis (RA). In addition, gut microbiota and its metabolites contribute to the occurrence and development of RA and obesity. However, the mechanism by which obesity affects RA remains unclear. In this study, we aimed to investigate whether gut microbiota and their metabolites alter the effects of high fat diet (HFD) on the severity of collagen-induced arthritis (CIA) in mice.

Methods: Briefly, mice were divided into normal group (N), CIA model group (C), HFD group (T), and HFD CIA group (CT). Hematoxylin and Eosin staining(HE) and Safranin O-fast green staining were conducted, and levels of blood lipid and inflammatory cytokines were measured. 16S rDNA sequencing technique and liquid chromatography-mass spectrometry (LC-MS)-based metabolomics were performed to explore changes in the microbiota structure to further reveal the pathomechanism of HFD on CIA.

Results: HFD aggravated the severity of CIA in mice. The CT group had the highest proportion of microbial abundance of Blautia, Oscillibacter, Ruminiclostridium-9, and Lachnospiraceae UCG 006 at the genus level, but had a lower proportion of Alistipes. Additionally, the fecal metabolic phenotype of the combined CT group shows significant changes, with differential metabolites enriched in 9 metabolic pathways, including primary bile acid biosynthesis, arginine biosynthesis, sphingolipid metabolism, purine metabolism, linoleic acid metabolism, oxytocin signaling pathway, aminoacyl-tRNA biosynthesis, the pentose phosphate pathway, and sphingolipid signaling pathway. Correlation analysis revealed that some of the altered gut microbiota genera were strongly correlated with changes in fecal metabolites, total cholesterol (TC), triglyceride (TG), and inflammatory cytokine levels.

Conclusions: This study shows that HFD may aggravate inflammatory reaction in CIA mice by altering the gut microbiota and metabolic pathways.

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高脂肪饮食通过改变肠道微生物群落增加了胶原蛋白诱发的小鼠关节炎的严重程度。

研究目的研究表明，肥胖可能与类风湿性关节炎（RA）有关。此外，肠道微生物群及其代谢产物也会导致类风湿关节炎和肥胖的发生和发展。然而，肥胖影响 RA 的机制仍不清楚。本研究旨在探讨肠道微生物群及其代谢产物是否会改变高脂饮食（HFD）对小鼠胶原诱导性关节炎（CIA）严重程度的影响：方法：将小鼠分为正常组（N）、CIA 模型组（C）、HFD 组（T）和 HFD CIA 组（CT）。对小鼠进行血红素和伊红染色（HE）和沙弗林 O-快绿染色，并测定血脂和炎症细胞因子的水平。通过16S rDNA测序技术和基于液相色谱-质谱联用技术（LC-MS）的代谢组学研究，探讨微生物群结构的变化，以进一步揭示HFD对CIA的病理机制：结果：HFD加重了小鼠CIA的严重程度。结果：HFD加重了小鼠CIA的严重程度。CT组的微生物丰度中，Blautia、Oscillibacter、Ruminiclostridium-9和Lachnospiraceae UCG 006的属级比例最高，但Alistipes的比例较低。此外，合并 CT 组的粪便代谢表型也发生了显著变化，在 9 个代谢途径中富集了不同的代谢物，包括初级胆汁酸生物合成、精氨酸生物合成、鞘脂代谢、嘌呤代谢、亚油酸代谢、催产素信号途径、氨基酰-tRNA 生物合成、磷酸戊糖途径和鞘脂信号途径。相关性分析表明，肠道微生物群属的一些改变与粪便代谢物、总胆固醇（TC）、甘油三酯（TG）和炎症细胞因子水平的变化密切相关：本研究表明，高氟日粮可能会通过改变肠道微生物群和代谢途径来加重 CIA 小鼠的炎症反应。

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

Advances in Rheumatology Medicine-Rheumatology

CiteScore

4.00

自引率

4.30%

发文量

审稿时长

53 weeks

期刊介绍： Formerly named Revista Brasileira de Reumatologia, the journal is celebrating its 60th year of publication. Advances in Rheumatology is an international, open access journal publishing pre-clinical, translational and clinical studies on all aspects of paediatric and adult rheumatic diseases, including degenerative, inflammatory and autoimmune conditions. The journal is the official publication of the Brazilian Society of Rheumatology and welcomes original research (including systematic reviews and meta-analyses), literature reviews, guidelines and letters arising from published material.