Overview

• Published in Nature Microbiology, the study shows that low, dynamic candidalysin output supports long-term oral colonization, whereas higher levels trigger inflammation and fungal clearance.
• In mice and keratinocyte assays, low-virulence strains transiently express ECE1, and ECE1 mutants cannot access terminally differentiated oral epithelial layers protected from IL-17–mediated defense.
• The laboratory strain SC5314 overproduces the toxin and is rapidly eliminated, while naturally occurring strain 101 produces little and persists without strong immune activation.
• The hyphal regulator EED1 governs filamentation and indirectly tunes candidalysin production, enabling the fungus to remain largely unnoticed in the oral mucosa.
• Teams in Zurich, Jena, and Paris combined targeted genetics, mouse infection models, and bioinformatics, and they note there are no immediate therapeutic applications for oral infections from these findings.