Evidence map›Paper›PMID 34297785›Full record

ArticlePLoS pathogens2021

Aryl hydrocarbon receptor activation by Lactobacillus reuteri tryptophan metabolism alleviates Escherichia coli-induced mastitis in mice.

Caijun Zhao, Xiaoyu Hu, Lijuan Bao, Keyi Wu, Lianjun Feng, Min Qiu, Haoyang Hao, Yunhe Fu, Naisheng Zhang

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
16.0field-weighted citation impact, top 1% of its field
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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Evaluation ofMicroorganisms · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. The Protective Effects and Underlying Mechanisms ofAnimals : an open access journal from MDPI · 2026
    Article
  12. Article
  13. Article
  14. Guardians within: Cross-talk between the gut microbiome and host immune system.World journal of gastrointestinal pathophysiology · 2025
    Review
  15. Disruption of Gut Microbiota-Mediated De Novo NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Anthocyanins Prevent Mastitis Exacerbation by Inhibiting PANoptosis Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article

15 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Caijun ZhaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Xiaoyu HuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Lijuan BaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Keyi WuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Lianjun FengDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Min QiuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Haoyang HaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.ORCID 0000-0003-4747-3369
Yunhe FuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.ORCID 0000-0002-3258-2610
Naisheng ZhangDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intestinal microbiota has been associated with the occurrence and development of mastitis, which is one of the most serious diseases of lactating women and female animals, but the underlying mechanism has not yet been elucidated. Aryl hydrocarbon receptor (AhR) activation by microbiota tryptophan metabolism-derived ligands is involved in maintaining host homeostasis and resisting diseases. We investigated whether AhR activation by microbiota-metabolic ligands could influence mastitis development in mice. In this study, we found that AhR activation using Ficz ameliorated mastitis symptoms, which were related to limiting NF-κB activation and enhancing barrier function. Impaired AhR activation by disturbing the intestinal microbiota initiated mastitis, and processed Escherichia coli (E. coli)-induced mastitis in mice. Supplementation with dietary tryptophan attenuated the mastitis, but attenuation was inhibited by the intestinal microbiota abrogation, while administering tryptophan metabolites including IAld and indole but not IPA, rescued the tryptophan effects in dysbiotic mice. Supplementation with a Lactobacillus reuteri (L. reuteri) strain with the capacity to produce AhR ligands also improved E. coli-induced mastitis in an AhR-dependent manner. These findings provide evidence for novel therapeutic strategies for treating mastitis, and support the role of metabolites derived from the intestinal microbiota in improving distal disease.

Indexed as

Limosilactobacillus reuteriAnimalsEscherichia coliEscherichia coli InfectionsFemaleGastrointestinal MicrobiomeMastitisMiceProbioticsReceptors, Aryl HydrocarbonTryptophanReceptors, Aryl HydrocarbonTryptophan

Identifiers

PMID34297785
PMCPMC8336809
OpenAlexW3186170263

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.