A role for Apolipoprotein A-I in the pathogenesis of multiple sclerosis

被引:23
|
作者
Meyers, Lindsay [1 ]
Groover, Chassidy J. [1 ]
Douglas, Joshua [1 ]
Lee, Sangmin [1 ,2 ]
Brand, David [1 ]
Levin, Michael C. [1 ,2 ]
Gardner, Lidia A. [1 ,2 ]
机构
[1] Res Serv VAMC, Memphis, TN 38104 USA
[2] Univ Tennessee, Hlth Sci Ctr, Dept Neurol, Memphis, TN 38163 USA
关键词
Multiple sclerosis; Apolipoprotein A-I; EAE; Neurological disease; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; TRANSCRIPTION FACTOR FOXP3; HIGH-DENSITY-LIPOPROTEIN; HIGH-DOSE SIMVASTATIN; REGULATORY T-CELLS; FLUORO-JADE-C; IL-23/IL-17; AXIS; TRANSGENIC MICE; MS-STAT; ATORVASTATIN;
D O I
10.1016/j.jneuroim.2014.10.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Apolipoprotein A1 (Apo A-I), the most abundant component of high-density lipoprotein (HDL), is an anti-inflammatory molecule, yet its potential role in the pathogenesis of multiple sclerosis (MS) has not been fully investigated. In this study, Western blot analyses of human plasma showed differential Apo A-I expression in healthy controls compared to MS patients. Further, primary progressive MS patients had less plasma Apo A-I than other forms of MS. Using experimental allergic encephalomyelitis (EAE) as a model for MS, Apo A-I deficient mice exhibited worse clinical disease and more neurodegeneration concurrent with increased levels of pro-inflammatory cytokines compared to wild-type animals. These data suggest that Apo A-I plays a role in the pathogenesis of EAE, a model for MS, creating the possibility for agents that increase Apo A-I levels as potential therapies for MS. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:176 / 185
页数:10
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