Effects of stress on immune function: the good, the bad, and the beautiful

Effects of stress on immune function: the good, the bad, and the beautiful
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DOI:
10.1007/s12026-014-8517-0
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发表时间:
2014-05-01
影响因子:
4.4
通讯作者:
Dhabhar, Firdaus S.
Dhabhar, Firdaus S.
中科院分区:
医学4区
文献类型:
--
作者:
Dhabhar, Firdaus S.

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虽然压力的概念已经赢得了不好的名声,但重要的是要认识到生理压力反应的适应性目的是促进在战斗或逃跑中的生存。虽然长期的压力通常是有害的,但短期的压力可以起到保护作用,因为它使生物体做好应对挑战的准备。这篇综述讨论了生物应激反应的免疫效应,可以引起心理,生理或物理(包括运动)的压力。我们提出,短期压力是自然界的基本但未被充分认识的生存机制之一,可以在临床上利用它来增强免疫保护。短期(即,持续数分钟至数小时)的应激增强了先天性/原发性和适应性/继发性免疫应答。免疫增强的机制包括树突状细胞、中性粒细胞、巨噬细胞和淋巴细胞运输、成熟和功能的变化以及局部和全身细胞因子的产生。相反,长期应激通过改变1型-2型细胞因子平衡、诱导低度慢性炎症以及抑制免疫保护细胞的数量、运输和功能来抑制或失调先天性和适应性免疫应答。慢性应激也可能通过抑制1型细胞因子和保护性T细胞以及增加调节/抑制性T细胞功能来增加对某些类型癌症的易感性。在这里,我们将免疫反应分为保护性,病理性或调节性,并讨论压力对健康的“好”与“坏”影响。因此,短期应激可以增强免疫保护性(伤口愈合、疫苗接种、抗感染剂、抗肿瘤)或免疫病理性(促炎、自身免疫)应答的获得和/或表达。相反,慢性应激可以抑制保护性免疫反应和/或加剧病理性免疫反应。研究,如这里讨论的那些可以提供机制的目标和概念框架的药理学和/或生物行为干预,旨在提高“好”的压力的影响,最大限度地减少“坏”的压力的影响,并最大限度地促进健康和愈合。
Although the concept of stress has earned a bad reputation, it is important to recognize that the adaptive purpose of a physiological stress response is to promote survival during fight or flight. While long-term stress is generally harmful, short-term stress can be protective as it prepares the organism to deal with challenges. This review discusses the immune effects of biological stress responses that can be induced by psychological, physiological, or physical (including exercise) stressors. We have proposed that short-term stress is one of the nature's fundamental but under-appreciated survival mechanisms that could be clinically harnessed to enhance immunoprotection. Short-term (i.e., lasting for minutes to hours) stress experienced during immune activation enhances innate/primary and adaptive/secondary immune responses. Mechanisms of immuno-enhancement include changes in dendritic cell, neutrophil, macrophage, and lymphocyte trafficking, maturation, and function as well as local and systemic production of cytokines. In contrast, long-term stress suppresses or dysregulates innate and adaptive immune responses by altering the Type 1-Type 2 cytokine balance, inducing low-grade chronic inflammation, and suppressing numbers, trafficking, and function of immunoprotective cells. Chronic stress may also increase susceptibility to some types of cancer by suppressing Type 1 cytokines and protective T cells and increasing regulatory/suppressor T cell function. Here, we classify immune responses as being protective, pathological, or regulatory, and discuss "good" versus "bad" effects of stress on health. Thus, short-term stress can enhance the acquisition and/or expression of immunoprotective (wound healing, vaccination, anti-infectious agent, anti-tumor) or immuno-pathological (pro-inflammatory, autoimmune) responses. In contrast, chronic stress can suppress protective immune responses and/or exacerbate pathological immune responses. Studies such as the ones discussed here could provide mechanistic targets and conceptual frameworks for pharmacological and/or biobehavioral interventions designed to enhance the effects of "good" stress, minimize the effects of "bad" stress, and maximally promote health and healing.