Evidence map›Paper›PMID 41305918›Full record

ArticleGut microbes2025

Antibiotic cocktail-induced changes in gut microbiota drive alteration of bile acid metabolism to restrain Th17 differentiation through the FXR-NLRP3 axis.

Yue Shao-Yu, Di Niu, Jia Chen, Wei-Yi Li, Xu Wang, Qing-Wei Meng, Wei-Jie Song, Yi-Ge Yang, Hui Wang, Rong-Rong Li and 8 more

Abstract read
In one paragraph

Article in Gut microbes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Review
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  7. Therapeutic effect ofFrontiers in pharmacology · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Yue Shao-YuDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Di NiuDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Jia ChenDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Wei-Yi LiDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Xu WangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Qing-Wei MengDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Wei-Jie SongDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Yi-Ge YangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Hui WangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Rong-Rong LiDepartment of Clinical Laboratory, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, People Republic of China.
Bo-Yang LiDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Li-Gang ZhangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Chao-Jie HuDepartment of Clinical Laboratory, The First Affiliated Hospital of USTC, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, Anhui, People Republic of China.
Ling-Fan XuDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Hui-Hui WangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Li ZhangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
Chao-Zhao LiangDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.
He-Xi DuDepartment of Urology, First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibiotics influence both gut microbial composition and immune regulation, but the detailed mechanisms are still undefined. Shifts in the microbiome caused by antibiotic exposure can modulate immune activity through various pathways. Therefore, we aimed to explore how antibiotics affect immune-inflammation by regulating Th17 cells through the gut microbiota of mice with experimental autoimmune prostatitis (EAP). Antibiotic-driven shifts in gut microbial communities and metabolite profiling in EAP mice were performed by integrating 16S rRNA sequencing with mass spectrometry-driven metabolomic analysis. Antibiotic cocktail (ABX) therapy mitigated EAP, modified the gut microbiome composition, and influenced bile acid metabolism. Fecal microbiota transplantation (FMT) using microbiota from ABX-treated feces into EAP mice effectively altered gut microbiome composition and alleviated disease symptoms, indicating that microbiome intervention reduces autoimmune inflammation and decreases deoxycholic acid (DCA) in mice. Subsequent experiments demonstrated that DCA suppresses farnesol X receptor (FXR) expression which can inhibit the NLRP3‒ IL17A axis, thus promoting Th17 cell development and exacerbating inflammatory cell infiltration of the prostate. Our initial clinical examination of patients with prostatitis and antibiotic treatment indicated that bile acid metabolism and Th17 cell development are affected by antibiotic therapy. This work revealed that antibiotic-induced gut microbiota dysbiosis decreases the bile acid metabolite DCA, further restraining Th17 cell differentiation via the FXR‒NLRP3 axis to alleviate autoimmune prostatitis. Our results reveal new perspectives regarding the interconnected dynamics of antibiotics, gut microbiota, bile acid metabolism, and immune regulation, with potential relevance for therapies targeting immune-mediated diseases.

Indexed as

Anti-Bacterial AgentsBile Acids and SaltsGastrointestinal MicrobiomeNLR Family, Pyrin Domain-Containing 3 ProteinProstatitisReceptors, Cytoplasmic and NuclearTh17 CellsAnimalsCell DifferentiationDisease Models, AnimalFecal Microbiota TransplantationHumansInterleukin-17MaleMiceMice, Inbred C57BLAnti-Bacterial AgentsBile Acids and SaltsInterleukin-17NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, Ribosomal, 16Santibioticbile acidFXRGut microbiotaprostatitisTh17 cell

Identifiers

PMID41305918
PMCPMC12667630

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.