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

Kumwenda, Pizga, Cottier, Fabien, Hendry, Alex C., Kneafsey, Davey, Keevan, Ben, Gallagher, Hannah, Tsai, Hung-Ji, Hall, Rebecca A. (2022) Oestrogen promotes innate immune evasion of Candida albicans through inactivation of the alternative complement system. Cell Reports, 38 (1). Article Number 110183. ISSN 2211-1247. (doi:10.1016/j.celrep.2021.110183) (KAR id:91778)

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Abstract

Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Factors that increase circulatory oestrogen levels like 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 oestrogen impacts the fungal host-pathogen interaction. Oestrogen promotes fungal virulence by enabling C. albicans to avoid the actions of the innate immune system. Oestrogen-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. Oestrogen 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.

Item Type: Article
DOI/Identification number: 10.1016/j.celrep.2021.110183
Uncontrolled keywords: Candida albicans, innate immune evasion, Factor H, hormone sensing, Gpd2
Subjects: Q Science
Q Science > QR Microbiology
Q Science > QR Microbiology > QR180 Immunology
Divisions: Divisions > Division of Natural Sciences > Biosciences
Depositing User: Becky Hall
Date Deposited: 08 Dec 2021 10:40 UTC
Last Modified: 23 Mar 2022 15:19 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/91778 (The current URI for this page, for reference purposes)
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