Expression of interleukin-16 by microglial cells in inflammatory, autoimmune, and degenerative lesions of the rat brain

被引:37
作者
Guo, LH
Mittelbronn, M
Brabeck, C
Mueller, CA
Schluesener, HJ
机构
[1] Univ Tubingen, Inst Brain Res, D-72076 Tubingen, Germany
[2] Univ Konstanz, Inst Mol Toxicol, D-78457 Constance, Germany
[3] Univ Bonn, Dept Neurosurg, D-53105 Bonn, Germany
关键词
interleukin-16; microglia; inflammation; autoimmunity; neurodegeneration; CNS;
D O I
10.1016/j.jneuroim.2003.09.017
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Here we report a comparative analysis of interleukin-16 (IL-16) expression by microglial cells of the normal rat brain in trimethyltin (TMT) neurotoxicity, experimental autoimmune uveitis (EAU), encephalomyelitis (EAE), and viral infection (Borna disease, Borna disease virus) by immunohistochemistry. Striking differences were observed. In contrast to the human brain, IL-16 was not expressed constitutively in the rat brain. Remote activation of microglial cells of the optic tract in EAU did not result into IL-16 expression. TMT intoxication induced expression in microglial cells of the hippocampus. In EAE and BDV, massive IL-16(+) microglial cells could be seen. Thus, IL-16 is a descriptor of microglial cell activation that discriminates between different disease models, and might be a valuable marker for the detection of microglia activation in human and rat central nervous system (CNS) diseases. (C) 2003 Elsevier B.V. All rights reserved.
引用
收藏
页码:39 / 45
页数:7
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