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Objective. Although studies indicate that Staphylococcus epidermidis (S. epidermidis) can regulate inflammation and anti-inflammatory cytokines, there is limited evidence supporting their effects on atopic dermatitis (AD). Here, we aimed to investigate the effects and potential mechanism of skin commensal bacteria on the immunity of mice with AD. Methods. Twenty-four female BALB/C mice were selected and divided randomly into 4 groups: normal group, atopic dermatitis model group (AD), atopic dermatitis/substrate group (AD/substrates), and atopic dermatitis/substrates/epidermidis group (AD/S. epidermidis). All the mice were given different ways. After 14 days, their skin conditions were scored, and the serum, ear tissue, and inguinal lymph node tissue were collected and analyzed. Furthermore, the flow cytometry was used to analyze the number of CD4°+°CD25°+°Foxp3°+°Treg in the mouse lymph node tissue. Results. Compared with the AD/substrate group, the mice ear thickness and dermatitis score were significantly reduced in the AD/S. epidermidis group; skin epidermis, acanthosis, the degree of keratinization, inflammatory cell infiltration in the dermis, and the number of mast cells were declined. The serum levels of IgE, IgG1, IgG2a, and TNF-α, IFN-γ, IL-4, and Eotaxin were significantly declined in the AD/S. epidermidis compared with the AD/substrate group. The proportion of CD4°+°CD25°+°Foxp3°+°Treg cells in the lymph node tissue was significantly increased in the AD/S. epidermidis group compared with the AD/substrate group. Conclusion. Staphylococcus epidermidis can regulate mice’s immune balance to alleviate AD-induced skin damage. |
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