应激系统通过 IL-17 信号通路加剧睡眠不足小鼠角膜擦伤后的炎症反应。

IF 7.9 2区 医学 Q1 IMMUNOLOGY
Yunxia Xue , Pengyang Xu , Yu Hu , Sijing Liu , Ruyu Yan , Shutong Liu , Yan Li , Jun Liu , Ting Fu , Zhijie Li
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引用次数: 0

摘要

睡眠不足(SD)对健康有广泛的不利影响。然而,SD 影响角膜病理生理学及其创伤后愈合的机制仍不清楚。本研究旨在检测睡眠不足小鼠角膜的基本生理特征,并确定角膜擦伤后损伤的病理生理反应。我们采用多平台水环境法作为 SD 模型,发现 SD 通过诱导交感神经系统和下丘脑-垂体-肾上腺轴的过度激活,导致角膜增殖、感觉和免疫平衡紊乱以及过度炎症反应和角膜擦伤后的延迟修复。角膜的病理生理变化主要是通过激活 IL-17 信号通路发生的。阻断肾上腺素能和糖皮质激素的合成以及局部中和 IL-17A 能显著改善 SD 处理小鼠的角膜稳态、过度炎症反应以及角膜损伤后的伤口修复延迟。这些结果表明,最佳的睡眠质量对角膜的生理平衡及其损伤后的修复过程至关重要。此外,这些观察结果还提供了潜在的治疗靶点,可通过抑制或阻断应激系统及其相关 IL-17 信号通路的激活来改善 SD 引起的角膜伤口修复延迟。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Stress systems exacerbate the inflammatory response after corneal abrasion in sleep-deprived mice via the IL-17 signaling pathway

Stress systems exacerbate the inflammatory response after corneal abrasion in sleep-deprived mice via the IL-17 signaling pathway

Sleep deprivation (SD) has a wide range of adverse health effects. However, the mechanisms by which SD influences corneal pathophysiology and its post-wound healing remain unclear. This study aimed to examine the basic physiological characteristics of the cornea in mice subjected to SD and determine the pathophysiological response to injury after corneal abrasion. Using a multi-platform water environment method as an SD model, we found that SD leads to disturbances of corneal proliferative, sensory, and immune homeostasis as well as excessive inflammatory response and delayed repair after corneal abrasion by inducing hyperactivation of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis. Pathophysiological changes in the cornea mainly occurred through the activation of the IL-17 signaling pathway. Blocking both adrenergic and glucocorticoid synthesis and locally neutralizing IL-17A significantly improved corneal homeostasis and the excessive inflammatory response and delay in wound repair following corneal injury in SD-treated mice. These results indicate that optimal sleep quality is essential for the physiological homeostasis of the cornea and its well-established repair process after injury. Additionally, these observations provide potential therapeutic targets to ameliorate SD-induced delays in corneal wound repair by inhibiting or blocking the activation of the stress system and its associated IL-17 signaling pathway.

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来源期刊
Mucosal Immunology
Mucosal Immunology 医学-免疫学
CiteScore
16.60
自引率
3.80%
发文量
100
审稿时长
12 days
期刊介绍: Mucosal Immunology, the official publication of the Society of Mucosal Immunology (SMI), serves as a forum for both basic and clinical scientists to discuss immunity and inflammation involving mucosal tissues. It covers gastrointestinal, pulmonary, nasopharyngeal, oral, ocular, and genitourinary immunology through original research articles, scholarly reviews, commentaries, editorials, and letters. The journal gives equal consideration to basic, translational, and clinical studies and also serves as a primary communication channel for the SMI governing board and its members, featuring society news, meeting announcements, policy discussions, and job/training opportunities advertisements.
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