Atopic dermatitis (AD), also known as atopic eczema, is chronic pruritic skin disease. AD can increase psychological stress as well, increasing glucocorticoid release and exacerbating the associated symptoms. Chronic glucocorticoid elevation disturbs neuroendocrine signaling and can induce neuroinflammation, neurotoxicity, and cognitive impairment; however, it is unclear whether AD‐related psychological stress elevates glucocorticoids enough to cause neuronal damage. Therefore, we assessed the effects of AD‐induced stress in a mouse AD model. AD‐related psychological stress increased astroglial and microglial activation, neuroinflammatory cytokine expression, and markers of neuronal loss. Notably, melatonin administration inhibited the development of skin lesions, scratching behavior, and serum IgE levels in the model mice, and additionally caused a significant reduction in corticotropin‐releasing hormone responsiveness, and a significant reduction in neuronal damage. Finally, we produced similar results in a corticosterone‐induced AD‐like skin model. This is the first study to demonstrate that AD‐related psychological stress increases neuroendocrine dysfunction, exacerbates neuroinflammation, and potentially accelerates other neurodegenerative disease states.

中文翻译：

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褪黑素可抑制NC / Nga特应性小鼠模型中特应性心理应激引起的神经元功能障碍与神经炎症相关

特应性皮炎（AD），也称为特应性湿疹，是慢性瘙痒性皮肤病。AD还可以增加心理压力，增加糖皮质激素的释放并加剧相关症状。慢性糖皮质激素升高会扰乱神经内分泌信号，并可能引起神经炎症，神经毒性和认知障碍。然而，尚不清楚与AD相关的心理压力是否使糖皮质激素升高到足以引起神经元损伤的程度。因此，我们评估了小鼠AD模型中AD诱导的应激的影响。与AD相关的心理压力增加了星形胶质细胞和小胶质细胞的激活，神经炎性细胞因子的表达以及神经元丢失的标志物。值得注意的是，褪黑激素的给药抑制了模型小鼠皮肤损伤的发展，抓挠行为和血清IgE水平，并显着降低促肾上腺皮质激素释放激素的反应能力，并显着减少神经元损伤。最后，我们在皮质类固醇诱导的AD样皮肤模型中产生了相似的结果。这是第一项证明与AD相关的心理压力会增加神经内分泌功能障碍，加剧神经炎症并可能加速其他神经退行性疾病状态的研究。