Conditioned medium from stem cells of human exfoliated deciduous teeth ameliorates mouse ovalbumin-specific allergic dermatitis

人脱落乳牙干细胞条件培养基可改善小鼠卵清蛋白特异性过敏性皮炎

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Abstract

BACKGROUND: Atopic dermatitis (AD), a chronic inflammatory skin disease, is characterized by intense itching and recurrent eczema-like lesions, requiring safer, more targeted therapies that modulate the immune response and restore skin barrier integrity. Conditioned medium derived from stem cells of human exfoliated deciduous teeth (SHED-CM) exhibits considerable immunomodulatory and regenerative effects. We evaluated the efficacy of SHED-CM in an AD-like mouse model and explored the underlying mechanisms. METHODS: Mice with ovalbumin (OVA)-specific allergic dermatitis (OSAD) were intravenously treated with SHED-CM, conditioned medium derived from fibroblast, or Dulbecco's Modified Eagle Medium, followed by antigen restimulation to induce AD-like dermatitis. Disease severity was assessed macroscopically and histologically. T cell phenotypes were analyzed using immunohistochemical staining, RT-qPCR, and flow cytometry. Total serum and OVA-specific immunoglobulin E (IgE) levels were measured using ELISA. Naïve splenic CD4⁺ T cells were activated using CD3/CD28 beads in SHED-CM to evaluate their direct effects on T cell differentiation through flow cytometry. Highly expressed proteins in SHED-CM were identified using liquid chromatography-mass spectrometry, and neutralizing antibodies were used to elucidate the therapeutic mechanisms. RESULTS: The treatment with SHED-CM significantly ameliorated AD-like symptoms, reduced epidermal hyperplasia, and restored filaggrin expression. SHED-CM created an anti-inflammatory microenvironment in OSAD skin and draining lymph nodes by promoting Treg differentiation and inhibiting Th2 and Th17 populations. SHED-CM markedly suppressed B cell maturation, antigen-specific IgE production, and mast cell activation. Furthermore, we found that SHED-CM directly promoted Treg differentiation from naïve CD4⁺ T cells stimulated by CD3/CD28, which was mediated, in part, through TGFβ contained in SHED-CM. SHED-CM exhibited little to no effect on in vitro Th1, Th2, and Th17 differentiation. CONCLUSIONS: SHED-CM shows significant therapeutic potential for AD-like symptom, effectively modulating immune response and enhancing skin barrier restoration. Our findings offer a new approach for developing novel, targeted therapies for inflammatory skin disorders.

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