CRITICAL ROLE OF GALECTIN-1 (GAL-1) DURING YERSINIA ENTEROCOLITICA INFECTION

DAVICINO, ROBERTO; ELIçABE, JAVIER; DI GENARO, SILVIA; RABINOVICH, GABRIEL A

Lima

Congreso; Inmunoperu 2012; 2012

Asociación Latinoamericana de Inmunologia (ALAI)

Yersinia enterocolitica (Ye) cause gastrointestinal infection. Galectin-1 (Gal-1), a â-galactoside-binding lectin widely expressed at sites of infection and inflammation, limits Th1 and Th17 responses. However, its participation in bacterial infection is unknown. We investigated the role of endogenous Gal-1 in the development of immunity against Ye. Wild-type (WT) and Gal-1 knockout (Lgals1-/-) mice were orally infected with Ye. Expression of Gal-1, mouse survival and weight, and colony forming units (CFU) in different organs were determined. IL-17 and IFN-ã were measured by ELISA. We found that Ye infection induced expression of Gal-1. Higher survival rate (63 % vs 37 %), higher weight (p <0.05) and augmented IFN-ã and IL-17 levels were observed in Lgals1-/- mice (p <0.05). CFU numbers increased in WT mice receiving anti-Gal-1 blocking antibody as well as in Lgals1-/- receiving recombinant Gal-1 (rhGal-1) (p<0.05). These results were consistent with the levels of IFN-ã and IL-17. Accordingly, Ye susceptibility was higher in mice treated with IL-17 and/or IFN-ã antibodies. Moreover, anti-Gal-1 treatment induced an increase in NF-kB translocation and TNF production (p<0.05), demonstrating the critical role of this endogenous lectin in driving an anti-inflammatory responses. Our results provide the first evidence of a role for Gal-1 in this bacterial infection.