Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Psychoneuroendocrinology. 2021 Jul;129:105240. doi: 10.1016/j.psyneuen.2021.105240. Epub 2021 Apr 28.
Sleep disturbances and insufficient sleep are highly prevalent. Both clinical sleep disorders and multiple forms of experimental sleep loss predict heightened inflammation. As such, it is necessary to investigate potential protective factors. Given that trait positive affect (PA) is associated with reduced inflammation, and buffers the proinflammatory effects of stress, it is possible that high trait positive affect might protect individuals from an inflammatory response to sleep disruption. The present study tested this hypothesis in an experimental sleep disruption paradigm with assessment of cellular inflammation.
Data were drawn from good sleeping adults (n = 79) who participated in a randomized, within-subjects crossover experiment comparing the effects of two nights of sleep disruption versus two nights of uninterrupted sleep. Stimulated monocytic production of intracellular proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) were assayed using flow cytometric methods and indexed as the percentage of monocytes expressing TNF, IL-6, or co-expressing both. Hypotheses were evaluated using linear mixed effects models.
Controlling for negative affect, body mass index, age, and sex, PA significantly moderated the associations between sleep condition and stimulated monocyte production of IL-6 (b = -1.03, t = -2.02, p = .048) and its co-expression with TNF (b = -0.93, t = -2.00, p = .049), such that inflammatory responses were blunted among those high in PA with increases principally among those low in PA. The effect on TNF was similar in terms of effect size, but marginally significant.
Activation of cellular inflammation in response to sleep disruption is buffered by PA independent of negative affect. Interventions that promote PA might protect persons from the inflammatory activation following sleep loss, with the potential to mitigate the adverse health consequences of sleep disturbance.
睡眠障碍和睡眠不足非常普遍。临床睡眠障碍和多种形式的实验性睡眠剥夺都预示着炎症加剧。因此，有必要研究潜在的保护因素。由于特质性积极情绪（PA）与炎症减轻有关，并缓冲了应激的促炎作用，因此，高特质性积极情绪可能会保护个体免受睡眠中断引起的炎症反应。本研究在实验性睡眠中断范式中测试了这一假设，并评估了细胞炎症。
数据来自睡眠良好的成年人（n=79），他们参加了一项随机、自身对照交叉实验，比较了两晚睡眠中断与两晚不间断睡眠的效果。使用流式细胞术方法检测刺激单核细胞内促炎细胞因子肿瘤坏死因子（TNF）和白细胞介素-6（IL-6）的产生，并将其作为表达 TNF、IL-6 或两者共表达的单核细胞的百分比进行索引。使用线性混合效应模型评估假设。
控制负性情绪、体重指数、年龄和性别后，PA 显著调节了睡眠状况与刺激单核细胞产生 IL-6（b=-1.03，t=-2.02，p=0.048）和其与 TNF 共表达（b=-0.93，t=-2.00，p=0.049）之间的关联，使得 PA 高的个体的炎症反应减弱，而 PA 低的个体的炎症反应增加。在 TNF 方面，效应大小相似，但具有边缘显著性。
PA 独立于负性情绪缓冲了睡眠中断后细胞炎症的激活。促进 PA 的干预措施可能会保护人们免受睡眠不足后的炎症激活，从而减轻睡眠干扰的不良健康后果。
