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Vulvovaginal candidiasis, caused primarily byCandida albicans , presents significant health issues for women of childbearing age. As a polymorphic fungus, the ability ofC. albicans to switch between yeast and hyphal morphologies is considered its central virulence attribute. Armed with new criteria for defining vaginitis immunopathology, the purpose of this study was to determine whether the yeast-to-hypha transition is required for the hallmark inflammatory responses previously characterized during murine vaginitis. Kinetic analyses of vaginal infection withC. albicans in C57BL/6 mice demonstrated that fungal burdens remained constant throughout the observation period, while polymorphonuclear leukocyte (PMN), S100A8, and interleukin-1β levels obtained from vaginal lavage fluid increased by day 3 onward. Lactate dehydrogenase activity was also positively correlated with increased effectors of innate immunity. Additionally, immunodepletion of neutrophils in infected mice confirmed a nonprotective role for PMNs during vaginitis. Determination of the importance of fungal morphogenesis during vaginitis was addressed with a two-pronged approach. Intravaginal inoculation of mice withC. albicans strains deleted for key transcriptional regulators (bcr1 Δ/Δ,efg1 Δ/Δ,cph1 Δ/Δ, andefg1 Δ/Δcph1 Δ/Δ) controlling the yeast-to-hypha switch revealed a crucial role for morphogenetic signaling through the Efg1 and, to a lesser extent, the Bcr1 pathways in contributing to vaginitis immunopathology. Furthermore, overexpression of transcription factorsNRG1 andUME6 , to maintain yeast and hyphal morphologies, respectively, confirmed the importance of morphogenesis in generating innate immune responsesin vivo . These results highlight the yeast-to-hypha switch and the associated morphogenetic response as important virulence components for the immunopathogenesis ofCandida vaginitis, with implications for transition from benign colonization to symptomatic infection.

Fungal Morphogenetic Pathways Are Required for the Hallmark Inflammatory Response during Candida albicans Vaginitis