Fleshner M, Johnson J D
Department of Integrative Physiology, University of Colorado-Bouler, CO 80309-0354, USA.
Int J Hyperthermia. 2005 Aug;21(5):457-71. doi: 10.1080/02656730500088211.
Exposure to acute physical and/or psychological stressors induces a cascade of physiological changes collectively termed the stress response. The stress response is demonstrable at the behavioural, neural, endocrine and cellular levels. Stimulation of the stress response functions to improve an organism's chance of survival during acute stressor challenge. The current review focuses on one ubiquitous cellular stress response, up-regulation of heat shock protein 72 (Hsp72). Although a great deal is known about the function of intra-cellular Hsp72 during exposure to acute stressors, little is understood about the potential function of endogenous extra-cellular Hsp72 (eHsp72). The current review will develop the hypothesis that eHsp72 release may be a previously unrecognized feature of the acute stress response and may function as an endogenous 'danger signal' for the immune system. Specifically, it is proposed that exposure to physical or psychological acute stressors stimulate the release of endogenous eHsp72 into the blood via an alpha1-adrenergic receptor-mediated mechanism and that elevated eHsp72 functions to facilitate innate immunity in the presence of bacterial challenge.
暴露于急性生理和/或心理应激源会引发一系列生理变化，统称为应激反应。应激反应在行为、神经、内分泌和细胞水平上均可表现出来。应激反应的激活有助于提高生物体在急性应激源挑战期间的生存几率。本综述聚焦于一种普遍存在的细胞应激反应，即热休克蛋白72（Hsp72）的上调。尽管在暴露于急性应激源期间，细胞内Hsp72的功能已为人熟知，但对于内源性细胞外Hsp72（eHsp72）的潜在功能却知之甚少。本综述将提出一个假说，即eHsp72的释放可能是急性应激反应中一个此前未被认识到的特征，并且可能作为免疫系统的内源性“危险信号”发挥作用。具体而言，有人提出，暴露于生理或心理急性应激源会通过α1-肾上腺素能受体介导的机制刺激内源性eHsp72释放到血液中，并且升高的eHsp72在细菌攻击存在的情况下有助于促进先天免疫。
