Candida auris Persists in Hair Follicles, Hijacks Immune Signaling
Drug-resistant Candida auris was found to persist in hair follicles by exposing chitin, triggering interferon-γ that suppresses skin defenses and creates a niche for fungal colonization. The post Candida auris Persists in Hair Follicles, Hijacks Immune Signaling appeared first on GEN - Genetic Engineering and Biotechnology News .
Candida auris, a multidrug-resistant yeast discovered in 2009, has caused deadly outbreaks worldwide, resulting in around 3,000 deaths annually in U.S. hospitals and long-term care facilities. The fungus is known to colonize human skin, yet the mechanisms behind this persistence are still unclear. To investigate, researchers compared Candida auris with Candida albicans, a common skin fungus typically cleared by the immune system swiftly.
By using mouse models, fungal and mouse genetics, immunology, single-cell RNA-seq, and volumetric quantitative confocal microscopy, they discovered that while C. albicans disappeared within days, C. auris persisted, hiding in hair follicles.
This study, published in the journal Science, reveals that Candida auris colonizes skin better than other fungi, setting the stage for invasion once the immune system is weakened. The fungus directly binds to hair follicles and exhibits a strong affinity for them. In contrast to C. albicans, which triggers a protective immune response, C. auris induces a type 1-skewed immune reaction, characterized by an expansion of type 1 conventional dendritic cells, type 1 cytotoxic T cells, and type 1 helper T cells, along with increased interferon-gamma production.
This interferon gamma signals to hair follicle keratinocytes, diminishing the expression of IL-17A-driven genes and programs essential for skin barrier function and antimicrobial defense.
Moreover, Candida auris remodels its exterior cell wall to expose more chitin, which triggers the release of interferon gamma around the hair follicle. This interferon gamma hinders the skin's antifungal defenses, including IL-17, while also slowing the natural replacement of hair follicle cells. Consequently, a buildup of damaged cells occurs, creating an ideal environment for C. auris to thrive.
The researchers propose potential targets for preventing C. auris persistence on the skin, such as drugs that shift the immune system away from interferon gamma signals toward IL-17, or drugs that block chitin, thereby preventing the fungus from amplifying interferon gamma signals.
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