Evidence map›Paper›PMID 39116526›Full record

ArticleRedox biology2024

EGCG drives gut microbial remodeling-induced epithelial GPR43 activation to lessen Th1 polarization in colitis.

Siyan Che, Beibei Qin, Kunfu Wu, Mingzhi Zhu, Han Hu, Can Peng, Zi Wang, Yulong Yin, Yaoyao Xia, Miaomiao Wu

Abstract read
In one paragraph

Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  18. Histone deacetylase in inflammatory bowel disease: novel insights.Therapeutic advances in gastroenterology · 2025
    Review
  19. Respiratory diseases and the gut microbiota: an updated review.Frontiers in cellular and infection microbiology · 2025
    Review
  20. Review
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

10 authors.

Siyan CheHunan Provincial Key Laboratory for the Products Quality Regulation of Livestock and Poultry, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China.
Beibei QinHunan Provincial Key Laboratory for the Products Quality Regulation of Livestock and Poultry, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China.
Kunfu WuHunan Provincial Key Laboratory for the Products Quality Regulation of Livestock and Poultry, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China.
Mingzhi ZhuKey Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, Hunan Agricultural University, Changsha, 410128, China.
Han HuInstitute of Apicultural Research/State Key Laboratory of Resource Insects, Chinese Academy of Agricultural Sciences, Beijing, 100093, China.
Can PengInstitute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, 410125, China.
Zi WangDepartment of Hematology, The Second Xiangya Hospital of Central South University; Molecular Biology Research Center, Center for Medical Genetics, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha 410011, China. Electronic address: 220144@csu.edu.cn.
Yulong YinHunan Provincial Key Laboratory for the Products Quality Regulation of Livestock and Poultry, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China; Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, 410125, China.
Yaoyao XiaCollege of Animal Science and Technology, Southwest University, Chongqing, 400715, China. Electronic address: yaoyaoxia20230750@swu.edu.cn.
Miaomiao WuHunan Provincial Key Laboratory for the Products Quality Regulation of Livestock and Poultry, College of Animal Science and Technology, Hunan Agricultural University, Changsha, Hunan, 410128, China. Electronic address: miaomiaowu0316@hunau.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modulation of immune microenvironment is critical for inflammatory bowel disease (IBD) intervention. Epigallocatechin gallate (EGCG), as a natural low toxicity product, has shown promise in treating IBD. However, whether and how EGCG regulates the intestinal microenvironment is not fully understood. Here we report that EGCG lessens colitis by orchestrating Th1 polarization and self-amplification in a novel manner that required multilevel-regulated intestinal microecosystem. Mechanistically, EGCG activates GPR43 on IEC to inhibit Th1 polarization dependently of short chain fatty acid (SCFA)-producing gut microbiota. Inhibition of GPR43 activity weakens the protective effects of EGCG on colitis development. Moreover, we confirm that fecal SCFAs and/or intestinal GPR43 are limited in patients with colitis and are correlated with Th1 cell number. Taken together, our study reveals an intestinal microenvironment-dependent immunoregulatory effects of EGCG in treating IBD and provides insight into mechanisms of EGCG-based novel immunotherapeutic strategies for IBD.

Indexed as

CatechinColitisGastrointestinal MicrobiomeReceptors, G-Protein-CoupledTh1 CellsAnimalsDisease Models, AnimalFatty Acids, VolatileHumansIntestinal MucosaMiceCatechinepigallocatechin gallateFatty Acids, VolatileFfar2 protein, mouseReceptors, G-Protein-CoupledEGCGGPR43Inflammatory bowel diseaseShort chain fatty acidsTh1 cells

Identifiers

PMID39116526
PMCPMC11363845

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.