Dehydroepiandrosterone selectively inhibits production of tumor necrosis factor α and interlukin-6 in astrocytes

被引:52
作者
Kipper-Galperin, M
Galilly, R
Danenberg, HD
Brenner, T
机构
[1] Hadassah Univ Hosp, Lab Neuroimmun, IL-91120 Jerusalem, Israel
[2] Hadassah Univ Hosp, Dept Neurol, IL-91120 Jerusalem, Israel
[3] Hadassah Univ Hosp, Dept Cardiol, IL-91120 Jerusalem, Israel
[4] Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, IL-91010 Jerusalem, Israel
关键词
D O I
10.1016/S0736-5748(99)00067-2
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Dehydroepiandrosterone (DHEA) is a native neurosteroid with immunomodulating activity. DHEA effectively protects animals from several viral, bacterial and parasitic infections and it was suggested that its age-associated decline is related with immunosenescence. In the present study we examined the ability of DHEA to inhibit the production of inflammatory mediators by mycoplasma-stimulated glial cells and to change the course of acute central nervous system (CNS) inflammatory disease bl vivo. Addition of DHEA (10 mu g/ml) markedly inhibited tumor necrosis factor alpha (TNF alpha) and interlukin-6 (IL-6) production (98 and 95%, respectively), whereas nitric oxide (NO) and prostaglandin E-2 (PGE(2)) production was not affected. However, daily administration of 0.5 mg DHEA to mice or 5 mg to rats did not change the clinical outcome of experimental autoimmune encephalomyelitis (EAE). (C) 1999 ISDN. Published by Elsevier Science Ltd. All rights reserved.
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页码:765 / 775
页数:11
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