Campisi Jay, Leem Ted H, Fleshner Monika
Department of Kinesiology and Applied Physiology, University of Colorado-Boulder, Campus Box 354, Boulder, CO 80309-0354, USA.
Physiol Behav. 2002 Nov;77(2-3):291-9. doi: 10.1016/s0031-9384(02)00861-2.
Exposure to acute stress modulates immune function. Most research regarding stress and immunity has described the deleterious effects of stress. Recent studies, however, indicate that acute stress enhances many features of innate immunity. For example, exposure to acute stress reduced the time required to resolve inflammation produced by subcutaneous injection of streptomycin-killed, benign bacteria. It is unclear if this change in inflammation would be advantageous to the organism if challenged with living, infectious bacteria. Thus, the current experiments examined the effect of acute stressor exposure on inflammation development and resolution after a naturalistic, live bacterial challenge. In addition, nitric oxide (NO), an important bactericidal mediator, was measured at the inflammatory site. Rats (F344) were exposed to acute stress (100, 5-s, 1.6 mA tailshocks) and subcutaneously injected with live Escherichia coli ( approximately 2.5 x 10(9) colony forming units [CFU]). Stressed rats attained their peak inflammatory size quicker, resolved their inflammation 10-14 days faster, experienced less bacterial-induced weight loss and released 300% greater NO at the inflammatory site than nonstressed controls. Thus, acute stress improved recovery from bacterially induced inflammation possibly due to local elevations in NO.
暴露于急性应激会调节免疫功能。大多数关于应激与免疫的研究都描述了应激的有害影响。然而，最近的研究表明，急性应激会增强固有免疫的许多特征。例如，暴露于急性应激可缩短皮下注射经链霉素杀死的良性细菌所引发炎症的消退时间。如果受到活的感染性细菌的攻击，这种炎症变化对机体是否有利尚不清楚。因此，当前的实验研究了在自然状态下受到活细菌攻击后，暴露于急性应激源对炎症发展和消退的影响。此外，还在炎症部位检测了一种重要的杀菌介质一氧化氮（NO）。将大鼠（F344）暴露于急性应激（100次、每次5秒、1.6毫安的尾部电击），并皮下注射活的大肠杆菌（约2.5×10⁹菌落形成单位[CFU]）。与未受应激的对照组相比，受应激的大鼠炎症峰值大小出现得更快，炎症消退时间提前10 - 14天，细菌诱导的体重减轻更少，且在炎症部位释放的NO比对照组多300%。因此，急性应激可能由于局部NO水平升高而改善了细菌诱导炎症后的恢复情况。
