Panerai A E, Sacerdote P, Bianchi M, Manfredi B
Department of Pharmacology, University of Milan, Italy.
Int J Clin Pharmacol Res. 1997;17(2-3):115-6.
Both CNS- and immunocyte(lymphocytes, splenocytes)-derived beta-endorphin is involved in immune responses to stress. We show in the rat that stress-induced immunodepression (decrease of mitogen-induced lymphocyte proliferation and NK activity) is present only after the administration of a stress paradigm that increases immunocyte-derived beta-endorphin, while this is absent when the concentrations of the opioid are not modified. Interestingly, plasma corticosterone levels were similarly elevated after stresses whether or not they suppress immune responses, thus suggesting a pivotal role of the opioid. The increase of immunocyte beta-endorphin and immunosuppression are similarly present also after the intracerebroventricular administration of interleukin 1, thus suggesting a role for this cytokine in stress responses. The modifications of immunocyte beta-endorphin concentrations and immune responses induced by stress and interleukin 1 are not affected by indomethacin, adrenalectomy or hypophysectomy, whereas they are completely blocked by a CRH antagonist and depletion of the serotoninergic or catecholaminergic systems. In conclusion, our results suggest that immune responses to stress are not uniquely linked to an activation of the HPA axis.
中枢神经系统和免疫细胞（淋巴细胞、脾细胞）衍生的β-内啡肽均参与对应激的免疫反应。我们在大鼠实验中发现，应激诱导的免疫抑制（丝裂原诱导的淋巴细胞增殖和自然杀伤细胞活性降低）仅在给予能增加免疫细胞衍生β-内啡肽的应激模式后才会出现，而当阿片类物质浓度未改变时则不存在这种情况。有趣的是，无论应激是否抑制免疫反应，应激后血浆皮质酮水平均同样升高，因此提示阿片类物质起关键作用。脑室内注射白细胞介素1后，免疫细胞β-内啡肽增加和免疫抑制同样会出现，因此提示该细胞因子在应激反应中起作用。应激和白细胞介素1诱导的免疫细胞β-内啡肽浓度变化及免疫反应不受吲哚美辛、肾上腺切除术或垂体切除术的影响，而促肾上腺皮质激素释放激素拮抗剂以及血清素能或儿茶酚胺能系统耗竭则可完全阻断这些变化。总之，我们的结果提示，对应激的免疫反应并非唯一与下丘脑-垂体-肾上腺轴的激活相关。
