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

• DOI: 10.1007/s00109-015-1368-x
• Publication Date: 2015-12-02T04:21:31Z
• Authors: Hwei-Fang Tsai; Chien-Sheng Wu; Yi-Lin Chen; Hsiu-Jung Liao; I-Tsu Chyuan; Ping-Ning Hsu
• Keywords: Mice, Knockout; 0301 basic medicine; Galectin 3; Dextran Sulfate; Programmed Cell Death 1 Receptor; Forkhead Transcription Factors; Colitis; Severity of Illness Index; T-Lymphocytes, Regulatory; Lymphocyte Depletion; 3. Good health; Inducible T-Cell Co-Stimulator Protein; Disease Models, Animal; Mice; 03 medical and health sciences; Phenotype; T-Lymphocyte Subsets; Animals; Humans; Intestinal Mucosa; Biomarkers

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.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.