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Peer-reviewedCC BY 4.0Frontiers in Immunology

Tripterygium wilfordii ameliorates complete freund adjuvant-induced rheumatoid arthritis through modulating the gut-joint axis

  • Caili Zhang1,2
  • Qingru Chen1,2
  • Zheng Sun1,2
  • Tiantian Wu1,2
  • Yujie Zhang1,2
  • Binbin Huang3
  • Shenghai Huang4
  • Yan Zhang5
  • Maozhen Han1,2
5 affiliations
  1. 1School of Life Sciences, Anhui Medical University
  2. 2Microbial medicinal resources development research team, Anhui Provincial Institute of Translational Medicine
  3. 3School of Public Health, Anhui Medical University
  4. 4Department of Microbiology, The Key Laboratory of Microbiology and Parasitology of Anhui Province, The Key Laboratory of Zoonoses of High Institutions in Anhui, School of Basic Medical Sciences, Anhui Medical University
  5. 5School of Life Sciences, Hefei Normal University
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Abstract

Introduction: Although Tripterygium wilfordii (TW) is a classical Chinese herbal medicine for the treatment of rheumatoid arthritis (RA), the mechanism by which it alleviates inflammation through modulation of the gut microbiota remains unclear.

Methods: To elucidate the mechanism underlying the therapeutic effects of TW on RA, we first employed network pharmacology to predict the relevant pathways and core targets. Subsequently, an integrative multi-omics approach was applied, including gut metagenomics, gut metabolomics, serum metabolomics, and synovial transcriptomics, to investigate the alterations in gut microbiota, intestinal and serum metabolites, and synovial gene expression in a rat model of RA.

Results: Our findings revealed that TW supplementation lowered serum concentrations of IL-6, IL-1β, TNF-α, and IL-10 and modulated the Th17/Treg balance in intestinal tissue. TW treatment altered gut microbiota (GM) composition, marked by increased abundance of Prevotella sp PCJ2 and Psychrobacter pasteurii , and decreased Adlercreutzia equolifaciens and Schaedlerella arabinosiphila , synergizing with keystone species ( Bifidobacterium animalis, Phocaeicola sartorii, Blautia faecis ) to promote gut health. Concurrently, TW elevated tryptophan metabolites (tryptophol, tryptamine, 5-hydroxykynurenamine) while reducing 4-(2-aminophenyl)-2,4-dioxobutanoic acid, restoring tryptophan metabolism. This regulation coincided with upregulated Inmt mRNA in synovium, activating the tryptophan pathway. Correlation and mediation analyses indicated that gut-derived circulating metabolites such as N-myristoyl arginine and lauramidoxide were positively correlated with synovial Jun expression, potentially participating in the modulation of the IL-17-NF-κB cascade. Consistently, upregulated synovial Socs3 may exert negative feedback suppression on JAK-STAT signaling to alleviate inflammatory responses.

Discussion: These findings point to the gut microbiome and tryptophan pathway as a new therapeutic avenue for RA.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026tripterygium,
  title = {{Tripterygium wilfordii ameliorates complete freund adjuvant-induced rheumatoid arthritis through modulating the gut-joint axis}},
  author = {Caili Zhang and Qingru Chen and Zheng Sun and Tiantian Wu and Yujie Zhang and Binbin Huang and Shenghai Huang and Yan Zhang and Maozhen Han},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1828110},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1828110/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Tripterygium wilfordii ameliorates complete freund adjuvant-induced rheumatoid arthritis through modulating the gut-joint axis
AU  - Caili Zhang
AU  - Qingru Chen
AU  - Zheng Sun
AU  - Tiantian Wu
AU  - Yujie Zhang
AU  - Binbin Huang
AU  - Shenghai Huang
AU  - Yan Zhang
AU  - Maozhen Han
PY  - 2026
DA  - 2026/10/08
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1828110
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1828110/full
AB  - Introduction: Although Tripterygium wilfordii (TW) is a classical Chinese herbal medicine for the treatment of rheumatoid arthritis (RA), the mechanism by which it alleviates inflammation through modulation of the gut microbiota remains unclear.  Methods: To elucidate the mechanism underlying the therapeutic effects of TW on RA, we first employed network pharmacology to predict the relevant pathways and core targets. Subsequently, an integrative multi-omics approach was applied, including gut metagenomics, gut metabolomics, serum metabolomics, and synovial transcriptomics, to investigate the alterations in gut microbiota, intestinal and serum metabolites, and synovial gene expression in a rat model of RA.  Results: Our findings revealed that TW supplementation lowered serum concentrations of IL-6, IL-1β, TNF-α, and IL-10 and modulated the Th17/Treg balance in intestinal tissue. TW treatment altered gut microbiota (GM) composition, marked by increased abundance of Prevotella sp PCJ2 and Psychrobacter pasteurii , and decreased Adlercreutzia equolifaciens and Schaedlerella arabinosiphila , synergizing with keystone species ( Bifidobacterium animalis, Phocaeicola sartorii, Blautia faecis ) to promote gut health. Concurrently, TW elevated tryptophan metabolites (tryptophol, tryptamine, 5-hydroxykynurenamine) while reducing 4-(2-aminophenyl)-2,4-dioxobutanoic acid, restoring tryptophan metabolism. This regulation coincided with upregulated Inmt mRNA in synovium, activating the tryptophan pathway. Correlation and mediation analyses indicated that gut-derived circulating metabolites such as N-myristoyl arginine and lauramidoxide were positively correlated with synovial Jun expression, potentially participating in the modulation of the IL-17-NF-κB cascade. Consistently, upregulated synovial Socs3 may exert negative feedback suppression on JAK-STAT signaling to alleviate inflammatory responses.  Discussion: These findings point to the gut microbiome and tryptophan pathway as a new therapeutic avenue for RA.
SN  - 1664-3224
ER  -