Zonghao You, Xiaoyan Zhang, Sujie Huang, Denghui Chen, Yifan Zhu, Gen Li, Xi Chen
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引用次数: 0
摘要
特应性皮炎(AD)是一种复杂的疾病,受皮肤微生物组改变和免疫失调的影响。尽管这些因素的作用已得到公认,但人们对不同微生物种群影响皮肤免疫的具体途径仍然了解不足。在分子水平上,AD 的发病机制涉及 IL-4、IL-17、干扰素-γ(IFN-γ)和 IL-10 等关键细胞因子,它们有助于 T 辅助细胞(Th)反应的失衡。重要的是,γ-δ(γδ)T 细胞产生这些细胞因子并浸润 AD 中受影响的上皮细胞,但人们对它们的研究还不够。本研究试图通过移植皮肤微生物群来调整外周和局部免疫环境,从而减轻小鼠的AD症状。通过采用 16S rRNA 测序,我们对小鼠模型的皮肤微生物组进行了表征。我们的研究结果表明,微生物群干预能显著降低 DNFB 诱导的 AD 小鼠的皮肤增厚和血清 IgE 水平。此外,皮肤微生物群的变化还调节了免疫细胞的动态变化,恢复了 Th1/Th2 的平衡并导致临床症状的改善。这些发现凸显了皮肤微生物群在形成免疫反应中的关键作用,从而将基于微生物群的疗法定位为一种潜在的AD治疗方法。
The influence of skin microbial ecology on γδ T-cell immune pathways in allergic dermatitis models in mice.
Atopic dermatitis is a complex disease influenced by alterations in the skin microbiome and immune dysregulation. Despite the recognized role of these factors, the specific pathways by which distinct microbial populations affect skin immunity remain insufficiently understood. On a molecular level, the pathogenesis of atopic dermatitis involves critical cytokines such as IL-4, IL-17, interferon-γ, and IL-10, which contribute to the imbalance in T helper cell responses. Importantly, gamma-delta (γδ) T cells, which produce these cytokines and infiltrate affected epithelial cells in atopic dermatitis, have been underexplored. This study seeks to alleviate atopic dermatitis symptoms in mice by adjusting both peripheral and local immune environments through the transplantation of skin microbiota. By employing 16S rRNA sequencing, we characterized the skin microbiome of the mouse model. Our results demonstrate that microbiota intervention significantly reduces skin thickening and serum IgE levels in DNCB-induced atopic dermatitis mice. Additionally, changes in skin microbiota modulated immune cell dynamics, restoring the T helper 1 / T helper 2 balance and leading to clinical improvement. These findings highlight the critical role of skin microbiota in shaping immune responses, positioning microbiota-based therapies as a potential treatment for atopic dermatitis.
期刊介绍:
JLB is a peer-reviewed, academic journal published by the Society for Leukocyte Biology for its members and the community of immunobiologists. The journal publishes papers devoted to the exploration of the cellular and molecular biology of granulocytes, mononuclear phagocytes, lymphocytes, NK cells, and other cells involved in host physiology and defense/resistance against disease. Since all cells in the body can directly or indirectly contribute to the maintenance of the integrity of the organism and restoration of homeostasis through repair, JLB also considers articles involving epithelial, endothelial, fibroblastic, neural, and other somatic cell types participating in host defense. Studies covering pathophysiology, cell development, differentiation and trafficking; fundamental, translational and clinical immunology, inflammation, extracellular mediators and effector molecules; receptors, signal transduction and genes are considered relevant. Research articles and reviews that provide a novel understanding in any of these fields are given priority as well as technical advances related to leukocyte research methods.