Estradiol impairs the Th17 immune response against <i>Candida albicans</i>

Miguel Relloso, Laura Aragoneses-Fenoll, Sandra Lasarte, Christelle Bourgeois, Gema Romera, Karl Kuchler, Ángel L. Corbí, María Ángeles Muñoz‐Fernández, César Nombela, José Luis Rodríguez‐Fernández,

Journal of Leukocyte Biology · 2011 · 50 citations · 34 references

Concepts

Abstract

Candida albicans is a commensal opportunistic pathogen that is also a member of gastrointestinal and reproductive tract microbiota. Exogenous factors, such as oral contraceptives, hormone replacement therapy, and estradiol, may affect susceptibility to Candida infection, although the mechanisms involved in this process have not been elucidated. We used a systemic candidiasis model to investigate how estradiol confers susceptibility to infection. We report that estradiol increases mouse susceptibility to systemic candidiasis, as in vivo and ex vivo estradiol-treated DCs were less efficient at up-regulating antigen-presenting machinery, pathogen killing, migration, IL-23 production, and triggering of the Th17 immune response. Based on these results, we propose that estradiol impairs DC function, thus explaining the increased susceptibility to infection during estrus.

References

34