Odio M, Goliszek A, Brodish A, Ricardo M J
Immunol Lett. 1986 Aug;13(1-2):25-31. doi: 10.1016/0165-2478(86)90121-5.
A pronounced impairment of mitogen-induced proliferation of splenic lymphocytes was observed in Fischer-344 male rats 1 month after termination of exposure of the animals to stress. The stress model used in these experiments was random schedules of a signaled, escapable electric foot-shock stress for 2-4 h/day over a period of 6 months. The magnitude of the observed immunosuppression correlated positively with the total, cumulative stress exposure received by the animals. The effect was not secondary to changes in the percentage of splenic T lymphocytes in stressed, compared to control rats. Also, at the time of sacrifice, plasma levels of corticosterone were comparable in experimental and control animals. Therefore, the immunosuppression observed 1 month after the last stress session cannot be attributed to pituitary-adrenocortical hyperactivity, at the time of sacrifice. These results provide the first evidence that stress-induced immunosuppression is not restricted to the period of exposure to the stress. This finding may contribute to a better understanding of the suggested association between stressful life events and increased susceptibility to disease in humans.
在Fischer-344雄性大鼠停止应激暴露1个月后，观察到丝裂原诱导的脾淋巴细胞增殖明显受损。这些实验中使用的应激模型是在6个月的时间里，每天2 - 4小时对动物进行有信号提示、可逃避的足部电击应激的随机安排。观察到的免疫抑制程度与动物所接受的总的、累积的应激暴露呈正相关。与对照大鼠相比，这种效应并非继发于应激大鼠脾T淋巴细胞百分比的变化。此外，在处死时，实验动物和对照动物的血浆皮质酮水平相当。因此，在最后一次应激结束1个月后观察到的免疫抑制不能归因于处死时垂体-肾上腺皮质的过度活跃。这些结果首次证明应激诱导的免疫抑制并不局限于应激暴露期。这一发现可能有助于更好地理解压力性生活事件与人类疾病易感性增加之间的假定关联。
