Tumor necrosis factor-α and interleukin-6 regulate secretion of brain-derived neurotrophic factor in human monocytes

被引:140
作者
Schulte-Herbrüggen, O
Nassenstein, C
Lommatzsch, M
Quarcoo, D
Renz, H
Braun, A
机构
[1] Fraunhofer Inst Toxicol & Expt Med, D-30625 Hannover, Germany
[2] Humboldt Univ, Dept Neurol, Charite, Berlin, Germany
[3] Univ Rostock, Dept Pneumol, D-18057 Rostock, Germany
[4] Humboldt Univ, Dept Pediat, Charite, D-13353 Berlin, Germany
[5] Univ Marburg, Dept Clin Chem & Mol Diagnost, D-35033 Marburg, Germany
关键词
BDNF; neurotrophins; neuroimmunology; IL-6; TNF-alpha; inflammation; monocytes;
D O I
10.1016/j.jneuroim.2004.10.026
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Activated macrophages have been shown to produce brain-derived neurotrophic factor (BDNF) in diseases such as multiple sclerosis (MS) or allergic bronchial asthma (BA). However, there is little data on BDNF regulation in these cells. We demonstrate that unstimulated human peripheral blood monocytes, but not lymphocytes, constitutively secrete BDNF. IL-6 and TNF-alpha specifically enhanced BDNF secretion in monocytes, whereas typical Th1 - and Th2-cytokines did not show any effect. None of the cytokines induced BDNF secretion in T- or B-cells. Thus, Our data provide evidence that IL-6 and TNF-alpha represent a specific link between monocyte infiltration and neuronal changes in inflammatory diseases. (c) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:204 / 209
页数:6
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