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

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 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.