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Oral Bacillus subtilis modulates immune responses and reduces clinical symptoms in a murine model of atopic dermatitis 2260134

Year: 2026
Type: article
Abstract: Introduction Allergic diseases like atopic dermatitis (AD) have risen with modern lifestyle changes affecting the microbiome. AD involves skin barrier dysfunction and immune dysregulation. Bacillus subtilis is Gram-positive bacterium that has been shown in a variety of inflammatory diseases to suppress inflammation. This study shows oral Bacillus subtilis protects against House Dust Mite (HDM)-induced AD by reducing clinical symptoms, epidermal thickness, mast cells, and increasing immunoglobulin A (IgA) and intestinal regulatory T cells (Tregs). Methods BALB/c mice received oral Bacillus subtilis or PBS and topical HDM to induce AD. Disease severity was assessed using clinical scoring, H&E staining for epidermal thickness, Toluidine Blue for mast cell infiltration, and ELISA for total and HDM-specific Immunoglobulins. Multiplex and ELISA were used for serum analysis. Flow Cytometry and RT-PCR were used to analyze Tregs. Results Bacillus subtilis treatment reduced clinical symptoms in a murine model of atopic dermatitis. Mice receiving B. subtilis showed lower lesion scores at weeks 3 and 7. While epidermal thickness and Th2-associated antibodies (IgG1, IgE) were unaffected, total IgA increased with B. subtilis treatment. B. subtilis prevented mast cell accumulation in HDM-induced lesions, and elevated intestinal Tregs expressing GATA3 and IL-10. Conclusion Oral administration of B. subtilis reduced clinical symptoms in HDM-induced atopic dermatitis. Protection occurred without lowering IgE or IgG1 but correlated with increased IgA and gut Tregs expressing IL-10 and GATA3. This study supports the value of beneficial microbes for preventing the development of atopic disease, and sheds light on the importance of the gut-skin axis. Funding Source n/a Topic Categories Mucosal and Regional Immunology (MUC)
Language: English
Subfield: Dermatology
Field: Medicine
Open Access status: bronze
OpenAlex ID: W7171554136
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