STRESS, EXERCISE AND INNATE IMMUNITY

有证据表明，暴露于急性压力（精神或身体）调节免疫反应。 虽然以前的研究主要集中在压力的免疫抑制作用上，但最近已经清楚地表明，急性压力源暴露可以增强和抑制免疫系统。 具体而言，有证据表明，急性应激源暴露刺激先天免疫的许多方面，如细菌炎症，发热，巨噬细胞/嗜中性粒细胞一氧化氮，促炎细胞因子和急性期蛋白质的解决。 应激诱导的先天免疫增强是“应激反应”的适应性组成部分。 有趣的是，体育活动或锻炼也被报道可以增强由压力刺激的先天免疫的相同方面。 此外，体力活动可以防止压力的免疫抑制作用。最近，我们已经报道，暴露于一个既定的动物模型的急性应激促进了决议的体内细菌的挑战。 将大鼠暴露于不可避免的尾部电击应激，并皮下注射E。大肠杆菌，解决炎症反应的细菌挑战近2天快于非应激对照。因此，鉴于体力活动既可以刺激先天功能的各个方面，又可以调节急性应激源暴露的免疫后果，我们有兴趣研究体力活动对压力诱导的细菌炎症消退增加的影响。 初步数据表明，在暴露于急性应激源之前，体力活动增强了应激对细菌炎症消退的刺激作用。 也就是说，在暴露于急性应激之前运动的大鼠比暴露于应激或单独运动的大鼠快3-4天完全解决细菌炎症。 因此，本提案的目的是表征解决细菌炎症所需时间的减少是否是由于细菌清除率的增加或其他炎症因子的减少。

There is evidence that exposure to acute stress (mental or physical) modulates immune responses. Although previous research has focused on the immunosuppressive effects of stress, more recently it has become clear that acute stressor exposure can potentiate, as well as suppress, the immune system. Specifically there is evidence that acute stressor exposure stimulates many aspects of innate immunity; such as, resolution of bacterial inflammation, fever, macrophage/neutrophil nitric oxide, proinflammatory cytokines, and acute phase proteins. The stress-induced potentiation of innate immunity is an adaptive component of the "stress response". Interestingly, physical activity or exercise has also been reported to potentiate the same aspects of innate immunity that are stimulated by stress. In addition, physical activity can prevent the immunosuppressive effects of stress. Recently, we have reported that exposure to an established animal model of acute stress facilitates the resolution of an in vivo bacterial challenge. Rats exposed to inescapable tailshock stress, and challenged subcutaneously with E. coli, resolve the inflammatory response to the bacterial challenge nearly 2 days faster than non-stressed controls. Thus, given that physical activity can both stimulate aspects of innate function, and modulate the immunological consequences of acute stressor exposure, we were interested in investigating what effect physical activity would have on the stress-induced increase in the resolution of bacterial inflammation. Preliminary data suggest that physical activity, prior to exposure to an acute stressor, potentiates the stimulatory effect of stress on bacterial inflammation resolution. That is, rats that exercised prior to exposure to acute stress completely resolved the bacterial inflammation 3-4 days faster than rats exposed to either stress or exercise alone. Thus, the goal of this proposal is to characterize whether the decreased time required to resolve bacterial inflammation is due to an increase in bacterial clearance or a decrease in other inflammatory factors.