Differential involvement of sympathetic nervous system and immune system in the modulation of TNF-α production by α2- and β-adrenoceptors in mice

被引:133
作者
Szelényi, J [1 ]
Kiss, JP [1 ]
Vizi, ES [1 ]
机构
[1] Hungarian Acad Sci, Inst Expt Med, Dept Pharmacol, H-1450 Budapest, Hungary
基金
匈牙利科学研究基金会;
关键词
tumor necrosis factor-alpha; cytokine; sympathetic nervous system; noradrenaline; endotoxaemia; neuroimmunomodulation; lipopolysaccharide;
D O I
10.1016/S0165-5728(99)00234-9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In the present study, the regulation of tumor necrosis factor-alpha (TNF-alpha) production by alpha(2)- and beta-adrenoceptors located on noradrenergic nerve terminals and on macrophages was studied in endotoxaemic mice. We found that reduction of the sympathetic outflow by reserpine dramatically increased the lipopolysaccharide (LPS)-induced TNF-alpha production, demonstrating that the release of endogenous noradrenaline (NA), controlled by presynaptic alpha(2)-adrenoceptors, was a determinant factor in this model. By using alpha(2)- and beta-adrenergic drugs (clonidine, CH-38083, isoproterenol, propranolol) we provided the first in vivo evidence that, beside the dominance of neuronal alpha(2)- and macrophage beta-adrenoceptors, the alpha(2)-adrenoceptors on macrophages were also involved in the modulation of LPS-induced TNF-alpha production. Since adrenergic drugs are widely used in the clinical practice, our findings may have therapeutical implications. (C) 2000 Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:34 / 40
页数:7
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