Melatonin restores DNFB-induced dysbiosis of skin microbiota in a mouse model of atopic dermatitis

• Published in: Life sciences (1973) 2024-04, Vol.342, p.122513-122513, Article 122513
• Main Authors: Yang, Kun, Yong, Jiang-yan, He, Yan, Yu, Lu, Luo, Gui-ning, Chen, Jilan, Ge, Yi-Man, Yang, You-jun, Ding, Wei-jun, Hu, Yi-mei
• Format: Article
• Language: English
• Subjects: Atopic dermatitis (AD); Epidermal microbiota; Intestinal microbiota; Melatonin (MLT); Staphylococcus aureus
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2024.122513

The epidermic microbiota plays crucial roles in the pathogenesis of atopic dermatitis (AD), a common inflammatory skin disease. Melatonin (MLT) has been shown to ameliorate skin damage in AD patients, yet the underlying mechanism is unclear. Using 2,4-dinitrofluorobenzene (DNFB) to induce an AD model, MLT intervention was applied for 14 days to observe its pharmaceutical effect. Skin lesions were observed using HE staining, toluidine blue staining and electron microscopy. Dermal proinflammatory factor (IL-4 and IL-13) and intestinal barrier indices (ZO1 and Occludin) were assessed by immunohistochemistry and RT–qPCR, respectively. The dysbiotic microbiota was analyzed using 16S rRNA sequencing. MLT significantly improved skin lesion size; inflammatory status (mast cells, IgE, IL-4, and IL-13); and the imbalance of the epidermal microbiota in AD mice. Notably, Staphylococcus aureus is the key bacterium associated with dysbiosis of the epidermal microbiota and may be involved in the fine modulation of mast cells, IL-4, IL-13 and IgE. Correlation analysis between AD and the gut revealed that intestinal dysbiosis occurred earlier than that of the pathological structure in the gut. Melatonin reverses DNFB-induced skin damage and epidermal dysbiosis, especially in S. aureus. Repeated administration of DNFB activates mast cells and induces the secretion of proinflammatory cytokines in skin tissue, ultimately leading to atopic dermatitis. Melatonin therapy reduces the number of mast cells, inhibits the secretion of IL-4 and IL-13 and the production of IgE, improves dermatitis symptoms and skin microbiota disorders, and reduces the abundance of S. aureus, thus inhibiting AD. [Display omitted]