Dowdell K C, Gienapp I E, Stuckman S, Wardrop R M, Whitacre C C
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine and Public Health, Columbus 43210-1239, USA.
J Neuroimmunol. 1999 Dec;100(1-2):243-51. doi: 10.1016/s0165-5728(99)00211-8.
Murine relapsing EAE can be profoundly suppressed by restraint stress (RST) administered beginning prior to neuroantigen immunization. This study determined what hormone pathway(s) mediate disease suppression. Our results showed that nadolol (NAD), a beta2-adrenergic antagonist, did not reverse the RST-induced suppression of EAE. However, administration of either RU486 or aminoglutethimide, which block the action of peripheral glucocorticoids, resulted in a partial reversal of EAE suppression. Administration of exogenous corticosterone mimicked the effects of RST, in terms of suppression of EAE, decrease in lymphoid cell numbers and decrease in Thl cytokine production. Therefore, the HPA axis plays a more profound role in the RST-induced suppression of EAE than does the sympathetic nervous system.
在神经抗原免疫之前开始施加的束缚应激（RST）可显著抑制小鼠复发性实验性自身免疫性脑脊髓炎（EAE）。本研究确定了介导疾病抑制的激素途径。我们的结果表明，β2肾上腺素能拮抗剂纳多洛尔（NAD）并未逆转RST诱导的EAE抑制。然而，给予阻断外周糖皮质激素作用的RU486或氨鲁米特会导致EAE抑制的部分逆转。就抑制EAE、减少淋巴细胞数量和降低Th1细胞因子产生而言，给予外源性皮质酮可模拟RST的作用。因此，与交感神经系统相比，下丘脑-垂体-肾上腺（HPA）轴在RST诱导的EAE抑制中发挥着更重要的作用。
