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Peer-reviewed veterinary case report

Alleviating effect of topical Paenibacillus polymyxa on Malassezia restricta-induced dermatitis by modulating immune response and skin microbiota.

Journal:
Microbial pathogenesis
Year:
2026
Authors:
Zhuang, Han-Xiao et al.
Affiliation:
College of Biosystems Engineering and Food Science · China

Abstract

Several studies have found that members of the fungal genus Malassezia can cause skin infections. The topical application of live bacteria has been proposed as a treatment for skin diseases by regulating the skin microbiota, receiving widespread attention in recent years. Therefore, this study screened Paenibacillus polymyxa JWYB12, which has prominent inhibitory capabilities against Malassezia restricta, using the agar plate diffusion method. Scanning electron microscopy revealed that P. polymyxa JWYB12 adhered to the surface of M. restricta, resulting in surface folding on M. restricta. When P. polymyxa JWYB12 was applied to a mouse model of M. restricta-induced dermatitis, their clinical symptoms improved, and reduced epidermal thickness and mast cell infiltration decreased. Enzyme-linked immunosorbent assays demonstrated that P. polymyxa JWYB12 downregulated pro-inflammatory factors associated with type 17 inflammation, including interleukins 1 beta (IL1B), 5 (IL6), 17A (IL17A), 17C (IL17C), 17F (IL17F) and 22 (IL22). Reverse transcription quantitative polymerase chain reactions indicated that P. polymyxa JWYB12 downregulated the expression of the aryl hydrocarbon receptor (Ahr) and cytochrome P450 family 1 subfamily A member 1 (Cyp1a1). Skin microbiota analyses suggested that P. polymyxa JWYB12 could alter β-diversity and reduce the relative abundance of M. restricta. These results demonstrated that P. polymyxa JWYB12 ameliorated M. restricta-induced dermatitis by modulating both the immune response and skin microbiota. This study provides supporting data and a theoretical basis for using topically applied live bacteria to promote skin health and balance the skin microbiota.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41759638/