Vulvovaginal candidiasis (VVC) is an infection that affects approximately 75% of women during their lifetime; 5% will develop the recurrent form (RVVC). The high incidence of RVVC might be attributable to powerful virulence factors of Candida albicans (Ca

RODRÍGUEZ E; MIRÓ MS; VIGEZZI C; ICELY PA; SOTOMAYOR CE

Buenos Aires

Congreso; IV LASID Meeting, LXIII Argentinean Immunology Society Meeting, II French-Argentinean Immunology Meeting,; 2015

LASID, Argentinean Immunology Society, French Society Immunology

Candida albicans is causal agent of Vulvovaginal candidiasis(VVC). Immunopathogenic response in VVC is governed by innate immune mediators. NLRP3-inflammasome activation by fungal components induces Caspase-1 activation, which cleaves proIL-1β into biologically active cytokine. Herein, we aimed to study the contribution of Caspase-1 pathway in the local response against attenuated virulence(AV) C.albicans strain(Ca) in a model of VVC. Ca ATCC-36801(Virulent-V) and AV-ATCC-36801 were used. Female C57BL/6(WT) and Caspase-1-/- mice in estrus phase (estradiol treated) were intravaginally inoculated with 5.106 Ca at day(D) 0. Estrogenized(E) and untreated mice were included as controls. At D2,4 and 8 of infection, vaginal lavage(VL) was obtained to evaluate the cell type present, fungal burden(CFU) and cytokine levels(ELISA) and vaginas and lumbar ganglia for histological studies. After Ca-V infection in WT-animals, VL was characterized by the presence of PMNC. The infection remained through the evaluated days; fungal forms were present in lumen and stratum corneum and associated with PMNC infiltrate and intraepithelial abscesses. The IL-1β was significantly diminished (D8) compared with WT-E group(p