Institute for Policy Research, Northwestern University, United States.
Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, United States; Cousins Center for Psychoneuroimmunology, University of California, Los Angeles, United States.
Psychoneuroendocrinology. 2019 May;103:147-155. doi: 10.1016/j.psyneuen.2018.11.026. Epub 2018 Dec 28.
Psychological stress and poor sleep are associated with a wide range of negative health outcomes, which are thought to be mediated in part by alterations in immune processes. However, the molecular bases of links among stress, sleep, and immune processes are not completely understood, particularly during adolescence when sensitivity to stress and problems with sleep tend to increase. In the current study, we investigated whether various stressors (daily stress, major life events, perceived stress), sleep indices (duration, efficiency), and their interactions (e.g., moderating effects) are associated with expression of genes bearing response elements for transcription factors that regulate inflammatory and anti-viral processes.
Eighty-seven late adolescents completed daily checklists of their social experiences across a 15-day period and reported on their major life events during the previous year. They also completed actigraphy-based assessments of sleep quality and duration during 8 consecutive nights. An average of 5.5 months later, participants reported on their global perceptions of stress during the previous month and provided blood samples for genome-wide expression profiling of mRNA from peripheral blood mononuclear cells (PBMCs).
Higher levels of daily interpersonal stress and shorter sleep duration were associated with upregulation of inflammation-related genes bearing response elements for proinflammatory transcription factor nuclear factor kappa B (NF-κB). Shorter sleep duration was also linked to downregulation of antiviral-related genes bearing response elements for interferon response factors (IRFs). Lastly, there was a significant interaction between daily stress and shorter sleep duration, such that the association between daily stress and inflammation-related gene expression was exacerbated in the context of shorter sleep duration. Results were independent of sex, ethnicity, parent education, body mass index, and smoking and alcohol history.
Everyday interpersonal stress and shortened sleep can be consequential for upstream NF-κB signaling pathways relevant to inflammatory processes during late adolescence. Notably, the occurrence of both may lead to even greater activation of NF-κB signaling.
心理压力和睡眠质量差与广泛的负面健康结果有关，这些结果被认为部分是通过免疫过程的改变来介导的。然而，压力、睡眠和免疫过程之间联系的分子基础尚不完全清楚，特别是在青少年时期，他们对压力的敏感性和睡眠问题往往会增加。在目前的研究中，我们调查了各种应激源（日常应激、重大生活事件、感知压力）、睡眠指数（持续时间、效率）及其相互作用（例如，调节作用）是否与调节炎症和抗病毒过程的转录因子的反应元件相关的基因表达有关。
87 名晚期青少年在 15 天的时间内完成了他们社交经历的日常清单，并报告了他们在前一年的重大生活事件。他们还在连续 8 个晚上完成了基于活动的睡眠质量和持续时间评估。大约 5.5 个月后，参与者报告了他们在前一个月的全球压力感，并提供了外周血单核细胞（PBMCs）的 mRNA 进行全基因组表达谱分析的血液样本。
较高水平的日常人际应激和较短的睡眠时间与炎症相关基因的上调有关，这些基因具有促炎转录因子核因子 kappa B（NF-κB）的反应元件。较短的睡眠时间也与抗病毒相关基因的下调有关，这些基因具有干扰素反应因子（IRFs）的反应元件。最后，日常应激和较短睡眠时间之间存在显著的相互作用，使得日常应激与炎症相关基因表达之间的关联在较短睡眠时间的情况下加剧。结果独立于性别、种族、父母教育程度、体重指数以及吸烟和饮酒史。
日常人际应激和睡眠时间缩短可能对青春期后期与炎症过程相关的 NF-κB 信号通路上游产生影响。值得注意的是，两者的发生可能会导致 NF-κB 信号的激活更加强烈。
