Stress and Immunosenescence: Protective Effects of Emotion Regulation

项目摘要 确定影响老年人年龄相关免疫功能障碍（免疫衰老）的因素， 对促进福祉和降低发病率至关重要-鉴于人口的迅速增长， 不断扩大的人口老龄化。观察和实验研究的证据表明，压力是 与老年人免疫功能较差有关。然而，人们对这一动态知之甚少。 （个体内变异）压力影响老年人的情绪和生理机制。 免疫功能此外，情绪调节可能是一种保护性因素，可以缓冲压力相关的 免疫衰老在以后的生活中，但在这方面的知识缺乏。此K99/R 00提案奠定了 一个独立的研究生涯的基础，专注于表征适应性情绪和 免疫机制有助于在压力下健康衰老。拟议的职业发展 计划将提供候选人：（1）在老龄化研究的理论和方法的专业知识，（2）先进的 免疫衰老和年龄相关的免疫变化的知识，以及（3）情绪和情感的训练 调节过程特别侧重于衰老和压力的背景。指导阶段利用 在肯塔基州大学（英国）和 跨学科指导团队的专业知识（英国：Segerstrom博士和Lutz博士;加州大学伯克利分校：Mauss博士; Penn州立大学：Dr. Ram，UCLA：Dr. Effros）。这些经验将补充候选人现有的 压力、情绪、健康和定量方法的背景。本研究有三个目的来检验 一个拟议模型的不同组成部分。目的1（K99）：研究情绪调节是否调节 生活压力与免疫衰老之间的联系。目标2（K99）：解释日常压力如何 与压力生物标志物升高有关，通过负面情绪的个体内变异性。目标3 (R00)：测试整个拟议的生物心理社会模型的适度调解途径。研究 采用了严格的方法，通过检查其相互作用的组件， 不同的时域（即，多年来发生的生活压力和日常麻烦，发生在一个更微观的 水平），在各种样本（社区居住的老年人和一个大的，全国代表性的样本），和 免疫衰老的几个标志物（淋巴细胞衰老，炎症，主要的促炎性 转录因子和可能驱动衰老的潜伏病毒）。同期和前瞻性滞后 使用多级建模和回归的缓和和调解模型将用于测试关系 在压力源中，对压力的情绪和生理反应，免疫衰老和情绪 调控最终，这个项目将增加对压力源的动态机制的理解， 影响老年人的免疫衰老以及情绪调节在促进健康衰老中的作用。

PROJECT SUMMARY Identifying factors that influence age-related immune dysfunction (immunosenescence) in older adults is central to promoting well-being and reducing morbidity – an increasing public health concern given the rapidly expanding aging population. Evidence from observational and experimental studies suggests that stress is associated with poorer immune function in older adults. However, less is known about the dynamic (intraindividual variability) emotional and physiological mechanisms by which stress influences older adults' immune function. In addition, emotion regulation may be a protective factor that can buffer stress-related immunosenescence in later life, but there is a dearth of knowledge in this area. This K99/R00 proposal lays the foundation for an independent research career focused on characterizing adaptive emotional and immunological mechanisms that contribute to healthy aging during stress. The proposed career development plan will provide the candidate: (1) expertise in theories and methodologies of aging research, (2) advanced knowledge in immunosenescence and age-related immune changes, and (3) training in emotion and emotion regulation processes focused specifically on contexts of aging and stress. The mentored phase capitalizes on substantial research and professional development resources at the University of Kentucky (UK) and the expertise of an inter-disciplinary mentoring team (UK: Dr. Segerstrom and Dr. Lutz; UC Berkeley: Dr. Mauss; Penn State University: Dr. Ram, UCLA: Dr. Effros). These experiences will supplement the candidate's existing background in stress, emotions, health, and quantitative methods. The present study has three aims to test different components of a proposed model. Aim 1 (K99): To examine whether emotion regulation moderates the association between life stressors and immunosenescence. Aim 2 (K99): To explain how daily stressors are associated with elevated stress biomarkers, through intraindividual variability in negative emotion. Aim 3 (R00): To test the moderated mediation pathways of the entire proposed biopsychosocial model. The research incorporates a rigorous approach to test the proposed model by examining its interacting components across different time domains (i.e., life stressors that occur over years and daily hassles that occur on a more micro level), in various samples (community-dwelling older adults and a large, nationally representative sample), and across several markers of immunosenescence (lymphocyte senescence, inflammation, a chief proinflammatory transcription factor, and a latent virus that may drive senescence). Concurrent and prospective lagged moderation and mediation models using multilevel modeling and regression will be used to test relationships among stressors, emotional and physiological responses to stress, immunosenescence, and emotion regulation. Ultimately, this project will increase understanding of the dynamic mechanisms by which stressors influence immunosenescence in older adults and the role of emotion regulation in promoting healthy aging.