# Role of Gut Microbiota and Metabolite Remodeling on the Development and Management of Rheumatoid Arthritis: A Narrative Review

**Authors:** Yichen Yu, Fulin Jin, Lijun Wang, Ji Cheng, Shifeng Pan

PMC · DOI: 10.3390/vetsci12070642 · Veterinary Sciences · 2025-07-05

## TL;DR

This review explores how gut microbiome imbalances contribute to rheumatoid arthritis and suggests that improving gut health could lead to new, low-risk treatments for both humans and animals.

## Contribution

The paper highlights the role of gut microbiota and metabolite changes in rheumatoid arthritis and proposes gut-targeted therapies as novel treatment strategies.

## Key findings

- Imbalances in gut microbiota weaken the intestinal barrier and promote systemic inflammation linked to rheumatoid arthritis.
- Probiotics and fecal microbiota transplantation show promise in improving gut health and reducing RA symptoms in animals.
- Targeting gut microbiota offers affordable and low-risk treatment options for rheumatoid arthritis in humans and livestock.

## Abstract

Rheumatoid arthritis is a chronic autoimmune disease that causes joint pain, inflammation, and disability in humans and animals, harming health and livestock productivity. This review explores the growing evidence linking rheumatoid arthritis to imbalances in the gut microbiome—the trillions of bacteria and microbes living in the intestines. The goal is to understand how these microbial changes contribute to rheumatoid arthritis and whether modifying the gut microbiome could offer new treatment strategies. Studies show RA patients and animals have fewer beneficial gut bacteria and more harmful bacteria. These imbalances weaken the gut barrier, allowing harmful substances to enter the bloodstream and spark systemic inflammation. The gut microbiome also disrupts immune balance, promoting damaging inflammation while reducing protective responses. Interventions like probiotics and fecal microbiota transplantation improved gut health and reduced rheumatoid arthritis symptoms in animal studies. By highlighting the gut–rheumatoid arthritis connection, this review suggests targeting gut health could provide affordable, low-risk treatments, especially for animals with limited therapies. The findings may inspire new probiotic products or personalized microbial treatments to prevent rheumatoid arthritis progression, benefiting both human patients and global livestock health.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that has a serious impact on both human health and animal production. The gut microbiota is a large and complex symbiotic ecosystem in animals, and the imbalance of gut microbiota is closely related to the pathogenesis of numerous diseases, including RA. The interactions among the gut microbiota, intestinal barrier, and immune system play key roles in maintaining intestinal homeostasis and affecting the development of RA. Regulating intestinal flora and metabolites provides new ideas for the prevention and treatment of RA. Probiotics can regulate the balance of intestinal flora and metabolites, improve the immune environment, and provide novel therapeutic strategies against RA. In order to summarize the role of gut microbiota and metabolite remodeling in the development and management of RA, this review will elaborate on the role of intestinal flora imbalance in the pathogenesis of RA and assess prospective therapeutic approaches that target the gut flora. Understanding the interaction among intestinal flora, metabolites, and RA will help to clarify the pathogenesis of RA and develop innovative and personalized therapeutic interventions against chronic autoimmune diseases.

## Linked entities

- **Diseases:** rheumatoid arthritis (MONDO:0008383)

## Full-text entities

- **Diseases:** RA (MESH:D001172), autoimmune disease (MESH:D001327)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

115 references — full list in the complete paper: https://tomesphere.com/paper/PMC12298641/full.md

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Source: https://tomesphere.com/paper/PMC12298641