Background

Although different studies associated sleep deprivation (SD) with systemic inflammatory changes, the effect of sleep duration on the pathology of allergic chronic diseases is poorly understood.

Objective

We sought to evaluate the influence of SD on allergen-induced pulmonary inflammation.

Methods

Ovalbumin (OVA)–sensitized C57BL/6 mice were exposed to a first set of intranasal OVA challenge under SD or healthy sleep (HS) conditions, followed by a second OVA challenge, 1 week apart. Some groups were subjected to corticosteroid treatment with dexamethasone.

Results

OVA-sensitized mice with SD had more severe airway inflammation than the allergic group with HS. Analysis of lung parenchyma revealed that the inflammation in allergic mice with SD was marked by an influx of neutrophils (mainly) and eosinophils and secretion of IL-6, TNF-α, and IL-17 in contrast to the eosinophilic inflammation and IL-4 production observed in allergic mice with HS. The same cytokine profile was observed in ex vivo culture of cervical lymph node cells and splenocytes, indicating that in allergic mice SD favors immune responses toward a proinflammatory T_H17 profile. This idea is supported by the fact that disruption of IL-17 signaling (IL-17 receptor A^−/−) prevented airway neutrophilia in allergic mice with SD. Furthermore, allergic mice with SD became refractory to corticosteroid treatment in contrast to the allergic group with HS.

Conclusion

Collectively, our data show that sleep quality participates in the progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refractory neutrophilic manifestation.

中文翻译：

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睡眠剥夺使变态反应性小鼠容易发生嗜中性肺炎

背景

尽管不同的研究将睡眠剥夺（SD）与全身性炎症改变相关联，但人们对睡眠持续时间对过敏性慢性疾病病理学的影响知之甚少。

客观的

我们试图评估SD对变应原诱发的肺部炎症的影响。

方法

卵清蛋白（OVA）致敏的C57BL / 6小鼠在SD或健康睡眠（HS）条件下接受第一组鼻内OVA攻击，然后隔1周进行第二次OVA攻击。一些组接受了地塞米松的皮质类固醇治疗。

结果

OVA敏感的SD小鼠比HS过敏组的气道炎症更严重。肺实质分析表明，SD变应性小鼠的炎症特征是嗜中性粒细胞和嗜酸性粒细胞大量涌入，而嗜酸性粒细胞炎症和IL-4则分泌IL-6，TNF-α和IL-17。在HS过敏性小鼠中观察到的生产。在子宫颈淋巴结细胞和脾细胞的离体培养中观察到相同的细胞因子谱，这表明在变态反应小鼠中SD有利于针对促炎性T _H 17谱的免疫反应。IL-17信号的破坏（IL-17受体A ^-/-）可预防SD过敏小鼠的气道中性粒细胞增多。此外，与HS过敏组相比，SD过敏小鼠对皮质类固醇激素治疗无效。

结论

总体而言，我们的数据表明睡眠质量参与了变应原诱导的嗜酸性粒细胞肺炎症发展为皮质类固醇难治性嗜中性粒细胞增多的过程。