IMMUNOMODULATORY EFFECT OF GALECTIN-1 IN A MODEL OF INFECTION WITH Yersinia enterocolitica.

VIGEZZI C; DAVICINO RC; DIAZ MS; DAVE MN; RABINOVICH GA; DI GENARO MS

Potrero de los Funes, San Luis

Congreso; XXX Reunión anual de la Sociedad de Biología de Cuyo; 2012

Sociedad de Biología de Cuyo

IMMUNOMODULATORY EFFECT OF GALECTIN-1 IN A MODEL OF INFECTION WITH Yersinia enterocolitica. Vigezzi C, Davicino RC, Diaz MS, Dave MN, Rabinovich GA. Di Genaro MS. Laboratory of Immunopathology, National University of San Luis, IMIBIO-SL (CONICET-UNSL), sdigena@unsl.edu.ar Yersinia enterocolitica (Ye) causes gastrointestinal infection. IFN-, a Th1 cytokine, is essential for the control of Ye infection. Th17 cytokines control pathogen dissemination from the mucosa. Galectin-1 (Gal-1), a β-galactoside-binding protein, limits Th1 and Th17 responses. The participation of Gal-1 in bacterial infection is unknown. We investigated the role of endogenous Gal-1 in the development of immunity against Ye. C57BL/6 wild-type (WT) and Gal-1 knockout (Lgals1-/-) mice were orally infected with 1?5 108 colony forming units (CFU) of Ye O:8 WA-314. Survival and weight of the mice, and bacterial load in Peyer´s patches (PP), mesenteric lymph nodes (MLN) and spleen were determined 5 days after infection. Gal-1 expression in the organs was studied by Western blot. IL-17 and IFN-γ levels were measured in homogenates of the organs by ELISA. We found that the infection induces Gal-1 expression in spleen. Although the weight was not significantly different from WT mice, higher survival rate (100 % vs 75%) was observed in Lgals1-/- mice after infection Augmented IL-17 levels were detected in PP, MLN and S of Lgals1-/- mice (p