Plasma-based strategy for inhibiting Candida albicans growth and CaMCA1 gene expression in vitro and reducing fungal pathogenicity in a murine model of vulvovaginal candidiasis.

Vulvovaginal candidiasis (VVC) is a common mucosal infection, mainly caused by Candida albicans. The use of common antifungal drugs in treatment of VVC is limited due to emergence of resistant fungal strains and severe side effects. Cold atmospheric plasma (CAP) as a novel therapeutic approach is proven to display strong antifungal activity against C. albicans. In the present study, the effects of CAP treatment on virulence and pathogenicity of C. albicans in a murine model was investigated. Candida albicans was treated with CAP at different time exposures. Fungal cell morphology and the expression profile of CaMCA1 gene in CAP-treated fungus was evaluated using electron microscopy and quantitative RT-PCR. Moreover, the mice model of VVC was developed using CAP-treated and non-treated C. albicans and characterized in terms of vaginal fungal burden, the rate of hyphae formation in the vaginal tissue and fluid and the inflammation degree of mice vaginal tissue. Significant reduction in CaMCA1 expression and remarkable mitochondrial degradation were observed in CAP-treated C. albicans cells. The lowest fungal burden, reduced hyphae formation, poor adherence of yeast cells to vaginal epithelium, and the low degree of inflammation were observed in mice infected with CAP treated C. albicans. Suppression of CaMCA1 gene and mitochondrial degradation in CAP-treated C. albicans yeast cells may diminish yeast to hyphae transition and reduce fungal pathogenicity in murine model of VVC. CAP treatment can be considered as a novel and efficient therapeutic strategy against C. albicans and related Candida infections in practice. LAY ABSTRACT CAP was successfully used to inhibit fungal growth and CaMCA1 gene expression in C. albicans. It caused morphological alterations in membranous structures of the yeast cells and finally led to the cell death. CAP meaningfully reduced C. albicans virulence and pathogenicity in a murine model of VVC.