Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis
Journal
Journal of Molecular Medicine
Journal Volume
94
Journal Issue
5
Pages
545-556
Date Issued
2016
Author(s)
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. ? 2015, Springer-Verlag Berlin Heidelberg.
Subjects
Galectin-3; Inflammatory bowel disease; Regulatory T cells
SDGs
Other Subjects
dextran sulfate; galectin 3; inducible T cell costimulator; programmed death 1 ligand 1; recombinant protein; transcription factor FOXP3; biological marker; dextran sulfate; forkhead transcription factor; Foxp3 protein, mouse; galectin 3; Icos protein, mouse; inducible T cell costimulator; programmed death 1 receptor; adoptive transfer; animal cell; animal experiment; animal model; animal tissue; Article; CD4+ T lymphocyte; cell infiltration; cell transfer; controlled study; disease severity; ex vivo study; experimental colitis; human; human cell; immunomodulation; mouse; nonhuman; protein expression; regulatory T lymphocyte; T cell depletion; weight reduction; animal; colitis; disease model; drug effects; genetics; immunology; intestine mucosa; knockout mouse; lymphocyte depletion; metabolism; pathology; phenotype; regulatory T lymphocyte; severity of illness index; T lymphocyte subpopulation; Animals; Biomarkers; Colitis; Dextran Sulfate; Disease Models, Animal; Forkhead Transcription Factors; Galectin 3; Humans; Inducible T-Cell Co-Stimulator Protein; Intestinal Mucosa; Lymphocyte Depletion; Mice; Mice, Knockout; Phenotype; Programmed Cell Death 1 Receptor; Severity of Illness Index; T-Lymphocyte Subsets; T-Lymphocytes, Regulatory
Publisher
Springer Verlag
Type
journal article