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<p>As an abundant fungal colonizer of mammalian skin, <i>Malassezia</i> establishes mutualistic or pathogenic interactions with the host. Here we show that <i>Malassezia furfur</i> promotes skin homeostasis by maintaining epidermal integrity via tryptophan-derived metabolites that activate the aryl hydrocarbon receptor (AhR), a key regulator of keratinocyte differentiation and inflammation. <i>M. furfur</i>-derived tryptophan derivatives activated AhR in human epidermal equivalents and upregulated proteins important for skin structure and barrier activity in mouse epidermis. In a mouse model of atopic dermatitis, <i>M. furfur</i> colonization with tryptophan supplementation reduced inflammation and restored barrier function, while a fungal mutant defective in indole production was unable to do so. Mice lacking AhR specifically in keratinocytes failed to benefit from <i>M. furfur</i>-mediated barrier protection. These findings establish a previously unrecognized mutualistic role for <i>Malassezia</i> in skin physiology and expand our understanding of the skin microbiota’s influence on barrier function and immune regulation.</p>

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Commensal yeast Malassezia produces tryptophan metabolites to promote tissue homeostasis via the aryl hydrocarbon receptor in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月19日

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  • Eduardo Gushiken-Ibañez,
  • Michelle Stokmaier,
  • Giuseppe Barone,
  • Alessia Staropoli,
  • Tugay Karakaya,
  • Hans-Dietmar Beer,
  • Francesco Vinale,
  • Giuseppe Ianiri,
  • Salomé LeibundGut-Landmann

摘要

As an abundant fungal colonizer of mammalian skin, Malassezia establishes mutualistic or pathogenic interactions with the host. Here we show that Malassezia furfur promotes skin homeostasis by maintaining epidermal integrity via tryptophan-derived metabolites that activate the aryl hydrocarbon receptor (AhR), a key regulator of keratinocyte differentiation and inflammation. M. furfur-derived tryptophan derivatives activated AhR in human epidermal equivalents and upregulated proteins important for skin structure and barrier activity in mouse epidermis. In a mouse model of atopic dermatitis, M. furfur colonization with tryptophan supplementation reduced inflammation and restored barrier function, while a fungal mutant defective in indole production was unable to do so. Mice lacking AhR specifically in keratinocytes failed to benefit from M. furfur-mediated barrier protection. These findings establish a previously unrecognized mutualistic role for Malassezia in skin physiology and expand our understanding of the skin microbiota’s influence on barrier function and immune regulation.