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间歇性而非连续性的不可逃避足部电击应激会影响大鼠的免疫反应和免疫细胞β-内啡肽浓度。

Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat.

作者信息

Sacerdote P, Manfredi B, Bianchi M, Panerai A E

机构信息

Department of Pharmacology, University of Milano, Italy.

出版信息

Brain Behav Immun. 1994 Sep;8(3):251-60. doi: 10.1006/brbi.1994.1023.

DOI:10.1006/brbi.1994.1023
PMID:7865896
Abstract

It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.

摘要

众所周知,多种应激源会影响免疫反应。阿片肽β-内啡肽(BE)深度参与应激反应,在免疫系统细胞中合成,并参与免疫功能的调节。我们分析了两种不同应激模式对大鼠免疫细胞中β-内啡肽浓度及免疫反应的调节能力。在暴露于不可逃避的间歇性足部电击(1.6 mA,60 Hz,1 s,每5 s一次,共20 min)后2小时和24小时,脾细胞、外周血单核细胞和淋巴结细胞中的β-内啡肽浓度显著升高。相比之下,暴露于持续3分钟的足部电击并未影响阿片肽的浓度。同样,仅在暴露于间歇性足部电击应激后,植物血凝素诱导的脾细胞增殖和自然杀伤活性才显著受损。相反,两种应激模式后血浆皮质酮水平均同样升高。促肾上腺皮质激素释放激素(CRH)受体拮抗剂预处理可防止应激诱导的免疫细胞BE增加和免疫抑制。总之,我们的数据表明,间歇性和持续性足部电击应激源激活不同的神经内分泌反应,且CRH在介导间歇性足部电击应激的免疫效应中起核心作用。文中讨论了β-内啡肽变化与免疫抑制之间的可能关系。

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