College of Medicine & College of Dentistry, Ohio State University, 4179 Postle Hall, 305 W. 12th. Ave., Box 18257, Columbus, Ohio 43218-2357.
Integr Comp Biol. 2002 Jul;42(3):556-64. doi: 10.1093/icb/42.3.556.
Stress may be defined as a sequence of events, that begins with a stimulus (stressor), that is recognized by the brain (stress perception), and which results in the activation of physiologic fight/flight/fright systems within the body (stress response). Many evolutionary selection pressures are stressors, and one of the primary functions of the brain is to perceive stress, warn the body of danger, and enable an organism to respond. We hypothesized that under acute conditions, just as the stress response prepares the cardiovascular and musculoskeletal systems for fight or flight, it may also prepare the immune system for challenges (e.g., wounding) which may be imposed by a stressor (e.g., an aggressor). Initial studies showed that acute (2h) stress induced a significant trafficking of immune cells to the skin. Since the skin is an organism's major protective barrier, we hypothesized that this leukocyte redistribution may serve to enhance skin immunity during acute stress. We tested this hypothesis using the delayed type hypersensitivity (DTH) reaction, which mediates resistance to various infectious agents, as a model for skin immune function. Acute stress administered immediately before antigen exposure significantly enhanced skin DTH. Adrenalectomy (ADX) eliminated the stress-induced enhancement of DTH while administration of physiological doses of corticosterone and/or epinephrine to ADX animals enhanced skin DTH in the absence of stress. These studies showed that changes in leukocyte distribution and circulating stress hormones are systemic mediators of the immunoenhancing effects of acute stress. We recently identified gamma interferon as a local cytokine mediator of a stress-induced immunoenhancement. Our results suggest that during acute stress the brain sends preparatory warning signals to the immune system just as it does to other fight/flight systems of the body.
压力可以被定义为一系列事件，这些事件始于大脑识别的刺激物（压力源），并导致身体内的生理战斗/逃跑/恐惧系统激活（压力反应）。许多进化选择压力都是压力源，大脑的主要功能之一是感知压力，警告身体有危险，并使生物体能够做出反应。我们假设，在急性情况下，正如压力反应为战斗或逃跑做好心血管和肌肉骨骼系统的准备一样，它也可能为可能由压力源（例如侵略者）施加的免疫挑战（例如，受伤）做好准备。最初的研究表明，急性（2 小时）压力会导致免疫细胞大量转移到皮肤。由于皮肤是生物体的主要保护屏障，我们假设这种白细胞重新分布可能有助于在急性压力下增强皮肤免疫力。我们使用迟发型超敏反应（DTH）反应作为皮肤免疫功能的模型来检验这一假设，该反应介导了对各种传染性病原体的抵抗力。在抗原暴露前立即给予急性压力会显著增强皮肤 DTH。肾上腺切除术（ADX）消除了压力引起的 DTH 增强，而向 ADX 动物给予生理剂量的皮质酮和/或肾上腺素在没有压力的情况下增强了皮肤 DTH。这些研究表明，白细胞分布和循环应激激素的变化是急性应激增强免疫的全身性介质。我们最近发现γ干扰素是应激诱导免疫增强的局部细胞因子介质。我们的结果表明，在急性压力下，大脑向免疫系统发送预备性警告信号，就像它向身体的其他战斗/逃跑系统发送信号一样。
