Kavelaars A, de Jong-de Vos van Steenwijk T, Kuis W, Heijnen C J
Department of Immunology, University Hospital for Children, Utrecht, The Netherlands.
Ann N Y Acad Sci. 1998 May 1;840:698-704. doi: 10.1111/j.1749-6632.1998.tb09608.x.
Juvenile chronic arthritis is associated with clinical symptoms indicating that there is a dysregulation of the sympathetic nervous system (SNS). Our data show that patients with juvenile chronic arthritis have an altered function of the SNS associated with increased central noradrenergic outflow, presumably leading to increased vasoconstriction, resulting in a decreased response to an orthostatic stressor. We also investigated the consequences of the altered reactivity of SNS for the reactivity of the immune system to mediators of the sympathetic nervous system and to glucorticoids. It appeared that leukocytes of these patients have an altered response to catecholamines. Triggering of the beta 2-adrenergic receptor leads to reduced cAMP responses that are due to the higher rate of cAMP degradation. In addition, catecholamines induce the production of IL-6 by leukocytes of these patients, via triggering of alpha 1-adrenergic receptors. Healthy controls do not express functional alpha 1-adrenergic receptors.
青少年慢性关节炎与临床症状相关,表明交感神经系统(SNS)存在调节异常。我们的数据显示,青少年慢性关节炎患者的SNS功能发生改变,伴有中枢去甲肾上腺素能流出增加,推测会导致血管收缩增强,从而对直立应激源的反应降低。我们还研究了SNS反应性改变对免疫系统对交感神经系统介质和糖皮质激素反应性的影响。这些患者的白细胞对儿茶酚胺的反应似乎发生了改变。β2 - 肾上腺素能受体的激活导致cAMP反应降低,这是由于cAMP降解速率较高所致。此外,儿茶酚胺通过触发α1 - 肾上腺素能受体,诱导这些患者白细胞产生IL - 6。健康对照者不表达功能性α1 - 肾上腺素能受体。