NEUROENDOCRINE AND IMMUNOLOGICAL MECHANISMS IN STRESS-INDUCED IMMUNOMODULATION
NEUROENDOCRINE AND IMMUNOLOGICAL MECHANISMS IN STRESS-INDUCED IMMUNOMODULATION
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DOI：
10.1016/0960-0760(91)90286-e
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发表时间：
1991-01-01
影响因子：
4.1
通讯作者：
DERIJK, R
中科院分区：
文献类型：
--
作者：
BERKENBOSCH, F;WOLVERS, DAW;DERIJK, R
在这里，我们报告了情绪压力源（约束，脚震）可以影响体液免疫反应以及免疫和辅助细胞分泌白细胞介素的能力。急性抑制应激（5分钟）可使脾抗体对绵羊红细胞的反应增强4- 6倍。为了研究内分泌机制，我们在大鼠体内培养了促肾上腺皮质激素释放因子（CRF）抗体。在应激暴露和免疫之前静脉注射这些抗体可以防止应激引起的体液反应的增加。在一项平行实验中，我们观察到crf免疫中和阻止了约束应激诱导的血浆ACTH浓度升高，但对血浆催乳素、刺激黑素细胞激素、肾上腺素和去甲肾上腺素反应没有影响。这些数据表明存在一种间接途径，包括ACTH和相关肽，CRF通过该途径控制应激的体液反应。我们将讨论免疫细胞水平上涉及CRF直接机制的途径。在一系列其他实验中，我们探讨了内毒素注射诱导的白介素-1和白介素-6血浆水平是否会受到情绪应激的调节。在内毒素注射前暴露于长时间的足部休克应激（20分钟）导致血浆ACTH和白细胞介素-1反应减弱，但不影响内毒素诱导的血浆白细胞介素-6反应。这些数据表明，情绪压力可能影响免疫功能的至少一个层面是通过改变免疫细胞产生或分泌免疫调节白介素的能力。
Here, we report that emotional stressors (restraint, footshock) can affect humoral immune responses as well as the capacity of immune and accessory cells to secrete interleukins. Acute restraint stress (5 min) caused a 4- to 6-fold enhancement of splenic antibody responses to sheep red blood cells. In an attempt to study endocrine mechanisms, we administered antibodies raised in rats to corticotropin releasing factor (CRF). Intravenous administration of these antibodies prior to stress-exposure and immunization prevented the stress-induced increase in the humoral response. In a parallel experiment, we observed that CRF-immunoneutralization prevented the restraint stress-induced increase in plasma ACTH concentrations, but was without effect on plasma prolactin, melanocyte stimulating hormone, adrenaline and noradrenaline responses. These data suggest the presence of an indirect pathway involving ACTH and related peptides by which CRF controls humoral responses to stress. A pathway involving a direct mechanism of CRF at the level of the immune cells will be discussed. In a set of other experiments, we addressed the question of whether interleukin-1 and interleukin-6 plasma levels induced by injection of endotoxin could be modulated by emotional stress. Exposure to prolonged footshock stress (20 min) prior to endotoxin injection resulted in a blunted plasma ACTH and interleukin-1 response, without affecting the endotoxin-induced plasma interleukin-6 response. These data suggest that at least one level at which emotional stress may influence immune function is by changing the capacity of immune cells to produce and or secrete immune regulatory interleukins.