Department of Immunophysiology, Institute of Physiology and Pathophysiology, Medical Faculty, Marburg, Germany.
Neuroimmunomodulation. 2010;17(3):165-8. doi: 10.1159/000258714. Epub 2010 Feb 4.
We studied whether, in parallel to the activity of the hypothalamus-pituitary-adrenal axis and the sympathetic nervous system, hypothalamic cytokine expression and monoaminergic neurotransmitter concentrations are affected during the development and chronification of arthritis induced by immunization of rats with type II collagen. Corticosterone levels were increased only transiently, and were even below the normal range as the disease progressed. Increased adrenaline blood levels and hypothalamic IL-1beta and IL-6 overexpression were observed only during the induction phase of the disease. The increase in hypothalamic noradrenaline content during the symptomatic phase was paralleled by a gradual loss of sympathetic fibers in the joints. Depletion of hypothalamic noradrenergic neurons at this time did not affect the symptomatology. Contrary to observations in healthy animals, no correlation between hypothalamic IL-1beta expression and noradrenaline content was observed in rats with arthritis. The dissociation between hypothalamic cytokine gene expression and noradrenergic neuronal activity, the lack of sustained stimulation of the stress axes, and the loss of sympathetic signals in the joints indicate that the communication between afferent immune messages to the central nervous system and two main efferent anti-inflammatory pathways under control of the brain are disrupted during experimental arthritis.
我们研究了在免疫接种 II 型胶原诱导的关节炎大鼠的下丘脑-垂体-肾上腺轴和交感神经系统活性的同时，下丘脑细胞因子表达和单胺能神经递质浓度是否受到影响。皮质酮水平仅短暂升高，随着疾病的进展甚至低于正常范围。仅在疾病诱导阶段观察到肾上腺素血液水平升高和下丘脑 IL-1β和 IL-6 过度表达。在症状期，下丘脑去甲肾上腺素含量的增加伴随着关节中交感神经纤维的逐渐丢失。此时，下丘脑去甲肾上腺素能神经元的耗竭并不影响症状。与健康动物的观察结果相反，在关节炎大鼠中，下丘脑 IL-1β表达与去甲肾上腺素含量之间没有相关性。下丘脑细胞因子基因表达和去甲肾上腺素能神经元活性之间的分离、应激轴的持续刺激缺乏以及关节中交感信号的丧失表明，在实验性关节炎期间，传入免疫信号与大脑控制的两个主要抗炎途径之间的中枢神经系统的通讯被破坏。
