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<p><i>Candida albicans</i> 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 <i>C. albicans</i>. Low-virulent strains of <i>C. albicans</i> expressed the candidalysin-encoding gene <i>ECE1</i> transiently upon exposure to keratinocytes in vitro. In mice, <i>ECE1</i> mutants were defective at accessing terminally differentiated oral epithelial layers where the fungus is protected from IL-17-mediated immune defence. Tight regulation of <i>ECE1</i> 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 <i>C. albicans</i> to create and maintain its niche in the oral mucosa.</p>

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Dynamic expression of candidalysin facilitates oral colonization of Candida albicans in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月25日

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  • Ricardo Fróis-Martins,
  • Julia Lagler,
  • Tim B. Schille,
  • Osama Elshafee,
  • Kontxi Martinez de San Vicente,
  • Sarah Mertens,
  • Michelle Stokmaier,
  • Iman Kilb,
  • Natacha Sertour,
  • Sophie Bachellier-Bassi,
  • Selene Mogavero,
  • Dominique Sanglard,
  • Christophe d’Enfert,
  • Bernhard Hube,
  • Salomé LeibundGut-Landmann

摘要

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.