Alterations of myelin proteins in inflammatory demyelination of BALB/c mice caused by Angiostrongylus cantonensis

被引:14
作者
Lin, K. Y. [2 ]
Chen, K. M. [1 ]
Lan, K. P. [3 ]
Lee, H. H. [1 ]
Lai, S. C. [1 ,4 ]
机构
[1] Chung Shan Med Univ, Dept Parasitol, Taichung 402, Taiwan
[2] Chung Shan Med Univ, Inst Med, Taichung 402, Taiwan
[3] CiShan Hosp, Dept Hlth, Dept Lab, Cishan Chen 842, Kaohsiung, Taiwan
[4] Chung Shan Univ Hosp, Clin Lab, Taichung 402, Taiwan
关键词
Angiostrongylus cantonensis; Demyelination; MAG; MBP; MOBP; PLP; CENTRAL-NERVOUS-SYSTEM; OLIGODENDROCYTIC BASIC-PROTEIN; PROTEOLIPID PROTEIN; MULTIPLE-SCLEROSIS; GENE-EXPRESSION; PLASMINOGEN ACTIVATORS; CEREBROSPINAL-FLUID; JIMPYMSD MICE; CNS MYELIN; EOSINOPHILS;
D O I
10.1016/j.vetpar.2010.03.019
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Angiostrongylus cantonensis causes eosinophilic meningitis or meningoencephalitis, yet little is known about demyelination caused by this parasite. To define the course of demyelination caused by A. cantonensis, we analyzed the expression of myelin proteins including myelin-associated glycoprotein (MAG), myelin basic protein (MBP), myelin-associated oligodendrocytic basic protein (MOBP), and proteolipid protein (PLP) in brain and cerebrospinal fluid (CSF)-like fluid of infected and uninfected BALB/c mice. In A. canronensis-infected mice, the expression of MAC, MBP, MOBP, and PLP mRNAs in brain tissue was decreased, while expression of the corresponding proteins was significantly increased in CSF-like fluid. Light microscopy revealed perivascular infiltrates in the brain during meningoencephalitis, suggesting that the cause of demyelination in angiostrongyliasis was immune system attack on the oligodendrocytic myelin sheath and subsequent release of myelin proteins into the CSF. Thus, intracerebral myelin breakdown in angiostrongyliasis may be a response to inflammatory mediators and the cause of increased myelin proteins in the CSF-like fluid. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:74 / 80
页数:7
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