Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat: involvement of corticotropin-releasing hormone, catecholamines, and serotonin.
Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat: involvement of corticotropin-releasing hormone, catecholamines, and serotonin.
复制标题
脑室内白细胞介素 1 α 增加大鼠免疫细胞 β-内啡肽浓度:促肾上腺皮质激素释放激素、儿茶酚胺和血清素的参与。
作者:
P. Sacerdote;M. Bianchi;B. Manfredi;A. Panerai
The opioid peptide beta-endorphin (BE) is synthesized and secreted by the cells of the immune system and has been shown to participate in the modulation of immune responses, e.g. during stress. Interleukin-1 (IL-1) is a potent activator of the corticotropin-releasing hormone (CRH) system in the hypothalamus, and it has been shown to be involved in many stress responses, including immunosuppression. We studied the effect of centrally injected IL-1 alpha on immunocyte BE concentrations in the rat. IL-1 alpha (1 ng/rat, intracerebroventricularly) significantly (P < 0.01) increased the concentrations of the peptide in splenocytes, lymph node cells, and peripheral blood mononuclear cells 2 and 24 h after treatment. Intracerebroventricular, but not iv, administration of 2 micrograms IL-1 receptor antagonist blocked the IL-1 alpha-induced increase. These effects were also prevented by the intracerebroventricular administration of the CRH receptor antagonist alpha-helical CRH-(9-41). Treatment with 6-hydroxydopamine and 5,7-dihydroxytryptamine, which deplete the catecholaminergic or the serotoninergic systems, respectively, blocked the increase in BE induced by the cytokine. In contrast, hypophysectomy and treatment with indomethacin did not modify the effect of IL. The increase in immunocyte BE, therefore, seems to depend on the activation of CRH, catecholamines, and serotonin, but to be independent of activation of the hypothalamus-pituitary-adrenal-axis and prostaglandins. The immunocyte BE increase could be involved in the immunosuppression induced by central IL-1 alpha.
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影响因子:
4.8
作者:
Katsuura,G;Gottschall,PE;Dahl,RR;Arimura,A
通讯作者:
Arimura,A
影响因子:
56.9
作者:
SAPOLSKY, R;RIVIER, C;VALE, W
通讯作者:
VALE, W
影响因子:
4.1
作者:
Chuluyan,HE;Saphier,D;Rohn,WM;Dunn,AJ
通讯作者:
Dunn,AJ
影响因子:
4.8
作者:
I. Kakucska;Yanping Qi;B. D. Clark;R. Lechan
通讯作者:
I. Kakucska;Yanping Qi;B. D. Clark;R. Lechan