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  • Estrogen promotes innate immune evasion of Candida albicans through inactivation of the alternative complement system.

Estrogen promotes innate immune evasion of Candida albicans through inactivation of the alternative complement system.

Cell reports (2022-01-06)
Pizga Kumwenda, Fabien Cottier, Alexandra C Hendry, Davey Kneafsey, Ben Keevan, Hannah Gallagher, Hung-Ji Tsai, Rebecca A Hall
ABSTRACT

Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Factors that increase circulatory estrogen levels such as pregnancy, the use of oral contraceptives, and hormone replacement therapy predispose women to VVC, but the reasons for this are largely unknown. Here, we investigate how adaptation of C. albicans to estrogen impacts the fungal host-pathogen interaction. Estrogen promotes fungal virulence by enabling C. albicans to avoid the actions of the innate immune system. Estrogen-induced innate immune evasion is mediated via inhibition of opsonophagocytosis through enhanced acquisition of the human complement regulatory protein, Factor H, on the fungal cell surface. Estrogen-induced accumulation of Factor H is dependent on the fungal cell surface protein Gpd2. The discovery of this hormone-sensing pathway might pave the way in explaining gender biases associated with fungal infections and may provide an alternative approach to improving women's health.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-Factor H Goat pAb, liquid, Calbiochem®
Sigma-Aldrich
Anti-Complement C3 Antibody, Chemicon®, from chicken
Sigma-Aldrich
Complement C3 from human serum, ≥3000 C3H50 units/mg (using C3 deficient serum)
Sigma-Aldrich
Anti-Complement C3b/iC3b Antibody, clone 6C9, clone 6C9, from mouse