title: Galectin-3 Modulates Experimental Colitis.
abstract: BACKGROUND
  We recently identified galectin-3 (gal-3) as a new and strong fibroblast activator produced by colonic epithelial cells. Very little is known about the influence of gal-3 in inflammatory bowel disease. We, therefore, investigated the impact of gal-3 on dextran sodium sulfate (DSS)-induced colitis in a mouse model.
  
  
  METHODS
  Colonic lamina propria fibroblasts of healthy controls were used for co-incubation studies of gal-3 with gal-1, TGF-β1, IFNγ, IL-4 and IL-10. Acute and chronic DSS colitis was induced by 3% DSS in drinking water in female Balb/c mice weighing 20-22 g. Recombinant gal-3 was expressed by the pET vector system and used for a 5-day treatment in different concentrations intraperitoneally. The distal third of the colon was used for histologic analysis. Colonic cytokine expression was determined by quantitative RT-PCR.
  
  
  RESULTS
  In vitro, gal-3 induced IL-8 secretion was significantly reduced by co-incubation with IL-10 (5 ng/ml) and IL-4 (10 ng/ml). Acute DSS-induced colitis was ameliorated by gal-3 treatment as indicated by increased colonic length and reduced weight loss compared to that of controls. In acute and chronic colitis, gal-3 treatment resulted in a significant suppression of colonic IL-6.
  
  
  CONCLUSIONS
  Gal-3 significantly reduces inflammation in acute and chronic DSS colitis in mice indicating a potential role in intestinal inflammation.
authors.affiliation: Department of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Lippert
authors.forename: Manuela
authors.initials: M
authors.lastname: Stieber-Gunckel
authors.forename: Nadja
authors.initials: N
authors.lastname: Dunger
authors.forename: Werner
authors.initials: W
authors.lastname: Falk
authors.forename: Florian
authors.initials: F
authors.lastname: Obermeier
authors.forename: Claudia
authors.initials: C
authors.lastname: Kunst
mesh_terms: D000208:Acute Disease; D000818:Animals; D001549:Benzamides / Q000378:metabolism; D002908:Chronic Disease; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D003106:Colon / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000187:drug effects* / Q000378:metabolism; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D037502:Galectin 3 / Q000096:biosynthesis / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D016753:Interleukin-10 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000187:drug effects / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D001549:Benzamides; D016207:Cytokines; D037502:Galectin 3; D015850:Interleukin-6; D016209:Interleukin-8; D016753:Interleukin-10; D015847:Interleukin-4; D014443:Tyrosine; C012614:1-nitrohydroxyphenyl-N-benzoylalanine; D016264:Dextran Sulfate