1. Paenibacillus exopolysaccharide alleviates Malassezia-induced skin damage: Enhancing skin barrier function, regulating immune responses, and modulating microbiota.
- Author
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Xie WY, Shen HL, Yan ZM, Zheng RJ, Jiang JJ, Zhong JJ, and Zhou WW
- Subjects
- Animals, Mice, Humans, Cytokines metabolism, Paenibacillus, Disease Models, Animal, HaCaT Cells, Malassezia drug effects, Skin microbiology, Skin drug effects, Skin immunology, Polysaccharides, Bacterial pharmacology, Microbiota drug effects
- Abstract
Numerous studies have established a strong association between Malassezia and various skin disorders, including atopic dermatitis. Finding appropriate methods or medications to alleviate Malassezia-induced skin damage is of notable public interest. This study aimed to evaluate the therapeutic effect of the exopolysaccharide EPS1, produced by Paenibacillus polymyxa, on Malassezia restricta-induced skin damage. In vitro assays indicated that EPS1 reduced the expression of pro-inflammatory cytokine genes in TNF-α-induced HaCaT cells. In a murine model, EPS1 was found to mitigate clinical symptoms, reduce epidermal thickness and mast cell infiltration, improve skin barrier function, decrease pro-inflammatory cytokine levels associated with type 17 inflammation, enhance Tregs in the spleen, upregulate the transcription of Treg-related genes in skin lesions, and modulate the skin microbiota. This study is the first to report the alleviating effect of Paenibacillus exopolysaccharide on Malassezia-induced skin inflammation and its impact on the skin microbiota. These findings support the potential of Paenibacillus exopolysaccharides as consumer products and therapeutic agents for managing Malassezia-induced skin damage by improving skin barrier function, modulating immune responses, and influencing skin microbiota., Competing Interests: Declaration of competing interest The authors declare that they do not possess any financial or commercial conflicts of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
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