Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression
Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression
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DOI：
10.1016/j.bbi.2007.07.010
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发表时间：
2007-11-01
影响因子：
15.1
通讯作者：
Schedlowski, Manfred
中科院分区：
文献类型：
--
作者：
Kemeny, Margaret E.;Schedlowski, Manfred
多年来，坊间证据和临床观察表明，暴露于社会心理压力可影响病毒感染、慢性自体免疫性疾病和肿瘤等免疫相关疾病的疾病结局。然而，缺乏支持这些观察结果的人体实验证据。近20年来发表在《脑、行为和免疫》等期刊上的研究表明，急性和慢性心理应激可引起先天和适应性免疫反应的显著变化，这些变化主要是通过下丘脑-垂体-肾上腺轴和交感神经-肾上腺轴的神经内分泌介质介导的。此外，心理压力还可以通过复杂的模型预测疾病结局，如病毒攻击、疫苗接种反应、疱疹病毒潜伏期追踪、肿瘤转移和实验伤口愈合的探索，以及疾病进展和死亡率的流行病学调查。这些研究极大地促进了我们对神经内分泌-免疫相互作用在许多病理生理条件下受到干扰的理解，应激可导致这种干扰，这些通信途径的故障可在疾病过程的进展中发挥重要作用。然而，在现存的文献中存在着重大的空白。在未来十年中，进一步分析疾病状态下的神经内分泌-免疫通讯，并确定中枢神经系统与控制重要疾病相关过程的分子事件之间的特定途径将是至关重要的。这些知识将为通过神经系统-免疫系统通讯的特定调节来治疗慢性疾病的新的治疗药理学和非药理学行为方法提供基础。(C) 2007爱思唯尔公司版权所有。
For many years, anecdotal evidence and clinical observations have suggested that exposure to psychosocial stress can affect disease outcomes in immune-related disorders such as viral infections, chronic autommume diseases and tumors. Experimental evidence in humans supporting these observations was, however, lacking. Studies published in the last 2 decades in Brain, Behavior and Immunity and other journals have demonstrated that acute and chronic psychological stress can induce pronounced changes in innate and adaptive immune responses and that these changes are predominantly mediated via neuroendocrine mediators from the hypothalamic-pituitaryadrenal axis and the sympathetic-adrenal axis. In addition, psychological stress has predicted disease outcomes using sophisticated models such as viral challenge, response to vaccination, tracking of herpesvirus latency, exploration of tumor metastasis and healing of experimental wounds, as well as epidemiological investigations of disease progression and mortality. These studies have contributed significantly to our understanding that the neuroendocrine-immune interaction is disturbed in many pathopbysiological conditions, that stress can contribute to this disturbance, and that malfunction in these communication pathways can play a significant role in the progression of disease processes. There are, however, significant gaps in the extant literature. In the coming decade(s), it will be essential to further analyze neuroendocrine-immune communication during disease states and to define the specific pathways linking the central nervous system to the molecular events that control important disease-relevant processes. This knowledge will provide the basis for new therapeutic pharmacological and non-pharmacological behavioral approaches to the treatment of chronic diseases via specific modulation of nervous system-immune system communication. (C) 2007 Elsevier Inc. All rights reserved.