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应激通过神经和激素机制抑制大鼠体内脾脏细胞因子的产生。

Stress-induced suppression of in vivo splenic cytokine production in the rat by neural and hormonal mechanisms.

作者信息

Meltzer Jonathan C, MacNeil Brian J, Sanders Veronica, Pylypas Susan, Jansen Arno H, Greenberg Arnold H, Nance Dwight M

机构信息

National Research Council of Canada Institute for Biodiagnostics, Winnipeg, MB, Canada R3E 0W3.

出版信息

Brain Behav Immun. 2004 May;18(3):262-73. doi: 10.1016/j.bbi.2003.09.003.

DOI:10.1016/j.bbi.2003.09.003
PMID:15050653
Abstract

The mechanisms mediating the effects of stress on immune function have yet to be fully described. In vitro studies have demonstrated a role for both the sympathetic nervous system (SNS) and the hypothalamic pituitary adrenal axis (HPAA) in regulating immune responses following exposure to various stressors. The purpose of the present set of experiments was to determine the in vivo contribution of the HPAA and SNS in regulating the effects of stress on lipopolysaccharide (LPS) induced splenic cytokine production. For this, rats with combinations of sham surgeries, splenic nerve cuts (SNC), and adrenalectomies (ADX) were exposed to 15 min of 1.6 mA intermittent footshock immediately following the intravenous (i.v.) injection of 0.1 microg of LPS. Although footshock was immunosuppressive to most indices of cytokine production, neither SNC nor ADX alone blocked the effects of stress on splenic immune function. However the combination of these two manipulations significantly abrogated the immunosuppressive effects of stress on cytokine production. Adrenal demedullation of animals with a SNC demonstrated that the SNS, not the HPAA, was primarily responsible for the immunosuppressive effects of stress.

摘要

介导应激对免疫功能影响的机制尚未完全阐明。体外研究表明,交感神经系统(SNS)和下丘脑-垂体-肾上腺轴(HPAA)在暴露于各种应激源后调节免疫反应中均发挥作用。本系列实验的目的是确定HPAA和SNS在体内对调节应激对脂多糖(LPS)诱导的脾脏细胞因子产生的影响所起的作用。为此,在静脉注射0.1微克LPS后,立即对接受假手术、脾神经切断(SNC)和肾上腺切除术(ADX)组合处理的大鼠施加15分钟的1.6毫安间歇性足部电击。尽管足部电击对大多数细胞因子产生指标具有免疫抑制作用,但单独的SNC或ADX均未阻断应激对脾脏免疫功能的影响。然而,这两种处理的组合显著消除了应激对细胞因子产生的免疫抑制作用。对接受SNC的动物进行肾上腺髓质剥除表明,主要是SNS而非HPAA对应激的免疫抑制作用负责。

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