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The fungal pathogen Candida auris exposes chitin to trigger IFNg and persist in hair follicles

ABSTRACT: Candida auris is an emerging multidrug-resistant fungus that has sparked public health alarm. However, the mechanisms supporting its persistence in skin, a major risk factor for deadly outbreaks, remain unclear. Here, we compared skin colonization by C. auris with that of the related pathobiont C. albicans, illuminating fungal–immune interactions. C. auris exhibited enhanced skin persistence, tropism to hair follicles, and direct binding to hair. Whereas C. albicans triggered a type 3/17-skewed sterilizing antifungal immune response, C. auris triggered a type 1 IFNg-driven response directed toward hair follicles. IFNg unexpectedly enhanced C. auris colonization through direct signaling to keratinocytes, impairing barrier integrity and repressing antifungal defense programs. Genetic and biochemical approaches demonstrated that, in response to skin-associated cues, C. auris upregulates the exposure of cell wall chitin, which is sufficient to trigger type 1 immunity and benefit the pathobiont.

ORGANISM(S): Mus musculus

PROVIDER: GSE328064 | GEO | 2026/08/10

REPOSITORIES: GEO

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The fungal pathogen Candida auris exposes chitin to trigger IFNg and persist in hair follicles [EDM_bulkRNA-seq]

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