Cambronero J C, Rivas F J, Borrell J, Guaza C
Cajal Institute, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Endocrinology. 1992 Aug;131(2):677-83. doi: 10.1210/endo.131.2.1639014.
The present work shows that interleukin-2 (IL-2) is able to increase in a dose-dependent manner (25-100 U/ml) CRF release from continuous perifused hypothalami. The effects of IL-2 and IL-1 on CRF secretion are potentiated by the simultaneous action of the two cytokines at the hypothalamus. The stimulatory effect of IL-2 on CRF secretion is significantly inhibited by the presence of dexamethasone in the perifusion medium. However, the CRF response to IL-2 was similar in adrenalectomized animals and sham-operated rats. It is suggested that the action of IL-2 on hypothalamic CRF secretion is integrated in the communication between the immune system and the hypothalamic-pituitary-adrenocortical axis, and that such action is subjected to glucocorticoid negative feedback modulation. The mechanism underlying the effect of IL-2 on CRF release is unknown, but arachidonic acid metabolites do not seem to be involved, since neither a lipooxygenase (nordihidrogueretic acid) nor a cyclooxigenase (indomethacin) inhibitor affected the hypothalamic secretory response to IL-2.
目前的研究表明，白细胞介素-2（IL-2）能够以剂量依赖性方式（25 - 100 U/ml）增加连续灌流的下丘脑释放促肾上腺皮质激素释放因子（CRF）。IL-2和IL-1对CRF分泌的作用在下丘脑通过两种细胞因子的同时作用而增强。灌流培养基中存在地塞米松时，IL-2对CRF分泌的刺激作用会被显著抑制。然而，肾上腺切除的动物和假手术大鼠对IL-2的CRF反应相似。这表明IL-2对下丘脑CRF分泌的作用整合于免疫系统与下丘脑 - 垂体 - 肾上腺皮质轴之间的通讯中，且这种作用受到糖皮质激素负反馈调节。IL-2对CRF释放作用的潜在机制尚不清楚，但花生四烯酸代谢产物似乎未参与其中，因为脂氧合酶抑制剂（去氢依托利酸）和环氧化酶抑制剂（吲哚美辛）均未影响下丘脑对IL-2的分泌反应。
