Analysis of the expression of galectins-1 and -3 in intestinal inflammatory disorders

RABINOVICH GA, MALDONADO CA, KOGAN Z, NIVELONI S, SAMBUELLI A, VAZQUEZ H, PEDREIRA S, SMECUOL E, NEGREIRA S, QUINTAR A, MAZURE R, MAURIÑO E, BAI JC

Chicago, USA

Congreso; DDW 2005. Digestive Diseases Week; 2005

American Association of Gastroenterology

Analysis of the expression of Galectins -1 and -3 in intestinal inflammatory disorders. Rabinovich GA, Maldonado CA, Kogan Z, Niveloni S, Sambuelli A, Vazquez H, Pedreira S, Smecuol E, Negreira S, Quintar A, Mazure R, Mauriño E, Bai JC. Immunogenetic Lab. Hospital de Clínicas, UBA. Centro de Microscopía Electrónica. School of Medicine, UNC. Gastroenterology Hospital; Buenos Aires, Argentina. Background: Inflammatory conditions of the intestines are consequence of a lack of tolerance to exogenous and endogenous antigens and a failure of the mucosal immune system with an imbalance of pro- and antiinflammatory factors. Galectins (Gal) are a family of sugar binding proteins, which are highly conserved throughout the evolution. At present, 15 Gal have been identified in different tissues including the immune system and the GI tract. Recent evidence indicates that Gal-1 and Gal-3 play a key role as regulators and tuners of the inflammatory response. Aim: to investigate the regulated expression of Gal-1 and Gal-3 in different intestinal inflammatory disorders including celiac sprue (CS), ulcerative colitis (UC) and Crohn’s disease (CD). Materials: Paraffin embedded sections from intestinal samples representing normal small bowel (n=10), normal colon (n=10), active CS (n=10), treated CS (n=10), active UC and CD were processed for immunogold staining. Results: Normal small intestine and colon had a weak expression of both Gal-1 and Gal-3, especially in the epithelium and lamina propria. While in active CS Gal-1 was also expressed at low levels, immunostaining was dramatically increased after specific treatment. There was no significant change in Gal-3 expression between untreated and treated patients. Regarding to UC, expression of both Gals was similar to controls. While there was a wide variability of staining between patients with CD, most samples showed a strong expression of both Gals at the level of inflammatory infiltrates and the epithelium. Conclusions: Our results suggest that the interplay between Gals-1 and –3 might play a role in regulating the inflammatory response in intestinal autoimmune disorders. The increased expression of Gal-1 in treated CS patients may represent an alternative mechanism of generating immune tolerance at the mucosal level.