Evidence map›Paper›PMID 26631140›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2016

Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis.

Hwei-Fang Tsai, Chien-Sheng Wu, Yi-Lin Chen, Hsiu-Jung Liao, I-Tsu Chyuan, Ping-Ning Hsu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
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  4. Dichotomous effects of Galectin-9 in disease modulation in murine models of inflammatory bowel disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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  15. Article
  16. Galectin-9 Is a Novel Regulator of Epithelial Restitution.The American journal of pathology · 2020
    Article
  17. Article
  18. ICOSFrontiers in immunology · 2020
    Review
  19. Article
  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

6 authors at 4 institutions in 1 country.

Hwei-Fang TsaiDepartment of Internal Medicine, Taipei Medical University Shuang Ho Hospital, New Taipei City, Taiwan.
Chien-Sheng WuDepartment of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Yi-Lin ChenGraduate Institute of Immunology, College of Medicine, National Taiwan University, 1 Jen-Ai Rd., Sec. 1, Taipei, 100, Taiwan.
Hsiu-Jung LiaoGraduate Institute of Immunology, College of Medicine, National Taiwan University, 1 Jen-Ai Rd., Sec. 1, Taipei, 100, Taiwan.
I-Tsu ChyuanDepartment of Internal Medicine, Cathay General Hospital, Taipei, Taiwan.
Ping-Ning HsuGraduate Institute of Immunology, College of Medicine, National Taiwan University, 1 Jen-Ai Rd., Sec. 1, Taipei, 100, Taiwan. phsu8635@ntu.edu.tw.
National Taiwan University · TWCathay General Hospital · TWFar Eastern Memorial Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledGalectin-3, a member of the β-galactoside-binding lectin family, expresses in many different immune cells and modulates broad biological functions including cell adhesion, cell activation, cell growth, apoptosis, and inflammation. However, the role of galectin-3 in mucosal immunity or inflammatory bowel diseases is still not clear. We demonstrate here that galectin-3 knockout mice have more severe disease activity in the dextran sulfate sodium (DSS)-induced colitis model, indicating that galectin-3 may protect from inflammation in DSS-induced colitis. Furthermore, treating with galectin-3 reduced body weight loss, shortened colonic length, and ameliorated mucosal inflammation in mice having DSS-induced colitis. However, the protective effects of galectin-3 were eliminated by the administration of anti-CD25 mAb. In addition, primary T cells treated with galectin-3 ex vivo induced the expression of FOXP3, ICOS, and PD-1 with a Treg cell phenotype having a suppression function. Moreover, adoptive transfer of galectin-3-treated T cells reduced bowel inflammation and colitis in the T cell transfer colitis model. In conclusion, our results indicate that galectin-3 inhibited colonic mucosa inflammation and reduced disease severity by inducing regulatory T cells, suggesting that it is a potential therapeutic approach in inflammatory bowel disease. KEY MESSAGES: Galectin-3 offers protection from inflammation in experimental colitis. Galectin-3 knockout mice have more severe disease activity in DSS-induced colitis. Adoptive transfer of galectin-3-treated T cells reduced bowel inflammation. Galectin-3 inhibited colonic mucosa inflammation by inducing regulatory T cells. Galectin-3 is a potential therapeutic approach in inflammatory bowel disease.

Indexed as

AnimalsBiomarkersColitisDextran SulfateDisease Models, AnimalForkhead Transcription FactorsGalectin 3HumansInducible T-Cell Co-Stimulator ProteinIntestinal MucosaLymphocyte DepletionMiceMice, KnockoutPhenotypeProgrammed Cell Death 1 ReceptorSeverity of Illness IndexBiomarkersDextran SulfateForkhead Transcription FactorsFoxp3 protein, mouseGalectin 3Icos protein, mouseInducible T-Cell Co-Stimulator ProteinProgrammed Cell Death 1 ReceptorGalectin-3Inflammatory bowel diseaseRegulatory T cells

Identifiers

PMID26631140
OpenAlexW2258385876

What OpenQuestion holds

Textmetadata
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.