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睡眠缺失与银屑病实验模型中的细胞因子水平。

Sleep loss and cytokines levels in an experimental model of psoriasis.

机构信息

Departamento de Psicobiologia, Universidade Federal de Sao Paulo, Sao Paulo, Brazil.

出版信息

PLoS One. 2012;7(11):e51183. doi: 10.1371/journal.pone.0051183. Epub 2012 Nov 30.

DOI:10.1371/journal.pone.0051183
PMID:23226485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3511390/
Abstract

Up to 80% of people develop a cutaneous condition closely connected to their exposure to stressful life events. Psoriasis is a chronic recurrent inflammatory skin disorder with multifactorial etiology, including genetic background, environmental factors, and immune system disturbances with a strong cytokine component. Moreover, psoriasis is variably associated with sleep disturbance and sleep deprivation. This study evaluated the influence of sleep loss in the context of an animal model of psoriasis by measuring cytokine and stress-related hormone levels. Male adult Balb/C mice with or without psoriasis were subjected to 48 h of selective paradoxical sleep deprivation (PSD). Sleep deprivation potentiated the activities of kallikrein-5 and kallikrein-7 in the skin of psoriatic groups. Also, mice with psoriasis had significant increases in specific pro-inflammatory cytokines (IL-1β, IL-6 and IL-12) and decreases in the anti-inflammatory cytokine (IL-10) after PSD, which were normalized after 48 h of sleep rebound. Linear regression showed that IL-2, IL-6 and IL-12 levels predicted 66% of corticosterone levels, which were selectively increased in psoriasis mice subject to PSD. Kallikrein-5 was also correlated with pro-inflammatory cytokines, explaining 58% of IL-6 and IL-12 variability. These data suggest that sleep deprivation plays an important role in the exacerbation of psoriasis through modulation of the immune system in the epidermal barrier. Thus, sleep loss should be considered a risk factor for the development of psoriasis.

摘要

高达 80%的人会出现一种与应激性生活事件密切相关的皮肤状况。银屑病是一种慢性复发性炎症性皮肤病,其病因包括遗传背景、环境因素以及免疫系统紊乱,并伴有强烈的细胞因子成分。此外,银屑病还与睡眠障碍和睡眠不足有关。本研究通过测量细胞因子和应激相关激素水平,评估了睡眠缺失在银屑病动物模型中的影响。有无银屑病的成年雄性 Balb/C 小鼠被剥夺选择性快动眼睡眠 48 小时。睡眠剥夺会增强银屑病组皮肤中激肽释放酶 5 和激肽释放酶 7 的活性。此外,银屑病小鼠在 PSD 后,特定促炎细胞因子(IL-1β、IL-6 和 IL-12)显著增加,抗炎细胞因子(IL-10)减少,而在 48 小时睡眠恢复后恢复正常。线性回归显示,IL-2、IL-6 和 IL-12 水平可预测皮质酮水平的 66%,而 PSD 后的银屑病小鼠皮质酮水平选择性增加。激肽释放酶 5 也与促炎细胞因子相关,可解释 66%的 IL-6 和 IL-12 变化。这些数据表明,睡眠剥夺通过调节表皮屏障中的免疫系统在银屑病恶化中起重要作用。因此,睡眠不足应被视为银屑病发展的一个风险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a60d/3511390/22faa064329d/pone.0051183.g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a60d/3511390/ef2d7c6519a3/pone.0051183.g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a60d/3511390/22faa064329d/pone.0051183.g007.jpg

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