CONICET | Buscador de Institutos y Recursos Humanos

Introduction:Candida albicans is a common commensal of mucosal surfaces and the most frequentcause of vulvovaginal candidiasis (VVC). The pathology affects 75% of all women at least once during their lifetime. Approximately 9% experience recurrent episodes of VVC (RVVC). This distressing condition is characterized by more than four episodes of VVC per year. Nowadays it is proposed that there is most likely a genetic component that contributes to the onset of RVVC. Pattern recognition receptors, such as Dectin-1, are essential determinants of host antifungal immunity. Dectin-1 is a major β-glucan receptor expressed on the surface of a variety of cells. This receptor recognizes β-1,3- glucans that are exposed on many fungi, including species of Candida.Objective:In this work we aimed to evaluate the susceptibility to vaginal Candida Infection in Dectin-1 Knockout (Dectin-1-/-) mice, focusing in the study of the early interactions between the fungus and local innate immune mechanisms.Methods:Female C57BL/6 mice (WT) and Dectin-1-/- were treated with estradiol on days (D) -6, - 3, 2, 4 and were intravaginally inoculated with 5.106 C. albicans SC5314 (D0) or only treated with estradiol (control). On D2, 4 and 8 vaginal lavages (VL) were performed to study the presence of different cell populations, fungal burden (CFU), IL-1β, TNF-α, IL- 17, IL-22 and IL-23 levels (ELISA) and vaginas were removed, sectioned and stained for histological analysis (PAS).Results:Dectin-1-/- mice were susceptible to the vaginal infection with higher CFU at D2 pi, and a progressive fungal burden reduction through D8, but without differences with WT mice. IL-1β, regarded as the hallmark of VVC immunopathogenesis, and TNF-α levels in VL were increased in infected animals of both strains, compared with controls during all evaluated D (p