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

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

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Abstract: Galectin-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.

Original languageEnglish
Pages (from-to)545-556
Number of pages12
JournalJournal of Molecular Medicine
Volume94
Issue number5
DOIs
Publication statusPublished - May 1 2016

Fingerprint

Galectin 3
Colitis
Inflammation
Dextran Sulfate
Regulatory T-Lymphocytes
Inflammatory Bowel Diseases
T-Lymphocytes
Adoptive Transfer
Knockout Mice
Mucous Membrane
Galactosides
Mucosal Immunity
Lectins
Cell Adhesion

Keywords

  • Galectin-3
  • Inflammatory bowel disease
  • Regulatory T cells

ASJC Scopus subject areas

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)

Cite this

Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis. / Tsai, Huei-Fang; Wu, Chien Sheng; Chen, Yi Lin; Liao, Hsiu Jung; Chyuan, I. Tsu; Hsu, Ping Ning.

In: Journal of Molecular Medicine, Vol. 94, No. 5, 01.05.2016, p. 545-556.

Research output: Contribution to journalArticle

Tsai, Huei-Fang ; Wu, Chien Sheng ; Chen, Yi Lin ; Liao, Hsiu Jung ; Chyuan, I. Tsu ; Hsu, Ping Ning. / Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis. In: Journal of Molecular Medicine. 2016 ; Vol. 94, No. 5. pp. 545-556.
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N2 - Abstract: Galectin-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.

AB - Abstract: Galectin-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.

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