GAL1 AND ITS SPECIFIC GLYCANS REGULATE MUCOSAL HOMEOSTASIS IN EXPERIMENTAL MODELS OF COLITIS

ANABELA MARÍA CUTINE ; MARTA ALICIA TOSCANO ; ROSA MARÍA MORALES ; GABRIEL ADRIÁN RABINOVICH ; LUCIANO GASTON MOROSI ; MARÍA MAY ; KARINA VALERIA MARIÑO

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

SAIC-SAIB-SAI-SAA-SAB-SAB-SAFE-SAFIS-SAH-SAP

Lectin-glycan interactions are crucial on many chronic inflammatory diseases. Galectin-1 (Gal1), a lectin that recognizes terminal N-acetyllactosamine in N- and O-glycans, can exert protective immunomodulatory activities in different chronic inflammation models, including TNBS-induced colitis in mice. However, the role of endogenous Gal1 in mucosal homeostasis and intestinal immunoregulation are still poorly understood. We evaluated the development of TNBS-induced colitis in C57BL/6 wild-type (WT) mice and in animals devoid of Gal1 (Lgals1-/-) or enzymes involved in the generation or masking of Gal1-glycoepitopes: Gcnt1 (generation of core-2 O-glycans) and St6gal1 (terminal α2,6 sialylation of N-glycans). Finally, we compared the development of colitis mediated by adoptive transfer of Gcnt1-/- or St6gal1-/- CD4+CD- 45BRhigh T cells in Rag2-/- mice. WT and Lgals1-/- mice developed acute TNBS-induced colitis, although with a more severe disease in Lgals1-/- animals (p