2026/06/19 by Eduardo Gushiken, Michelle Stokmaier, Giuseppe Barone +6 · 1 voice
Medicine · #Nail Diseases and Treatments #Dermatology and Skin Diseases #Acne and Rosacea Treatments and Effects
paper · pdf · doi:10.1038/s41564-026-02382-8
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.