Interaction Dectin-1/-glucans in brain: delicate balance between controlling inflammation and fungal control

VIGEZZI E, MIRÓ MS, RODRIGUEZ E, ICELY PA, SOTOMAYOR CE

Mar del Plata

Congreso; LIX Reunión anual de la Sociedad Argentina de Investigación Clínica y LXIV reunión científica anual de la Sociedad Argentina de Inmunología (SAI); 2016

LIX Reunión anual de la Sociedad Argentina de Investigación Clínica y LXIV reunión científica anual de la Sociedad Argentina de Inmunología (SAI)

Glucan receptor Dectin-1 is essential for antifungal response to Candida albicans in the periphery, but little is known about its role during Central Nervous System (CNS) infections. -glucans are widely recognized as immunomodulators. It has been demonstrated in vitro that the activation of microglia through Dectin-1 attenuates the production of proinflammatory cytokines. Our objective was to evaluate the role of this interaction in brain during C.albicans systemic infection. Male C57BL/6 mice were injected with 2,5.106 intra venous C.albicans SC5314 (parental) or SC5314-FKS 645 (glucan synthase mutant strain), and at 4,12,24 and 48h post-infection(pi). Animals were sacrificed and blood, kidney and brain samples were obtained to evaluate fungal burden (CFU), expression of Dectin-1 and IL-1beta (IL-1) (qPCR), and in situ cytokines secretion (IL-1, IL6, TNF-alpha, ELISA). Dectin-1 deficient mice (KO) were infected with SC5314 and killed at 4h and 12h. In both strain, fungemia was highest at 4h pi (CFU-p