Fróis-Martins Ricardo, Lagler Julia, Schille Tim B, Elshafee Osama, Martinez de San Vicente Kontxi, Mertens Sarah, Stokmaier Michelle, Kilb Iman, Sertour Natacha, Bachellier-Bassi Sophie, Mogavero Selene, Sanglard Dominique, d'Enfert Christophe, Hube Bernhard, LeibundGut-Landmann Salomé
Section of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Nat Microbiol. 2025 Oct;10(10):2472-2485. doi: 10.1038/s41564-025-02122-4. Epub 2025 Sep 25.
Candida albicans is a common fungal member of the human microbiota but can also cause infections via expression of virulence factors associated with the yeast-to-hyphae transition. The evolutionary selection pressure to retain these pathogenic traits for a commensal microorganism remains unclear. Here we show that filamentation and hyphae-associated factors, including the toxin candidalysin, are crucial for colonization of the oral cavity, a major reservoir of C. albicans. Low-virulent strains of C. albicans expressed the candidalysin-encoding gene ECE1 transiently upon exposure to keratinocytes in vitro. In mice, ECE1 mutants were defective at accessing terminally differentiated oral epithelial layers where the fungus is protected from IL-17-mediated immune defence. Tight regulation of ECE1 expression prevented detrimental effects of candidalysin on the host. Our results suggest that hyphae-associated factors such as candidalysin govern not only pathogenicity, but also mucosal colonization through direct host interactions enabling C. albicans to create and maintain its niche in the oral mucosa.