ArticleNature microbiology2026
Commensal yeast Malassezia produces tryptophan metabolites to promote tissue homeostasis via the aryl hydrocarbon receptor in mice.
Article in Nature microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Fourier transform infrared spectroscopy enables rapid strain typing inJournal of clinical microbiology · 2026Article
- Host skin lipids triggerbioRxiv : the preprint server for biology · 2026Article
- Fourier transform infrared spectroscopy enables rapid species discrimination acrossbioRxiv : the preprint server for biology · 2025Article
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Authors and funding
9 authors.
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Abstract
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.
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