Spinal cord histopathology of MOG peptide 35-55-induced experimental autoimmune encephalomyelitis is time- and score-dependent

被引:23
作者
Recks, Mascha S. [1 ]
Addicks, Klaus [1 ]
Kuerten, Stefanie [1 ]
机构
[1] Univ Cologne, Dept Anat 1, D-50931 Cologne, Germany
关键词
EAE; Histopathology; MOG:35-55; MS; Neurodegeneration; Staging; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; MULTIPLE-SCLEROSIS; AXONAL DAMAGE; C57BL/6; MICE; LESIONS; SPECIFICITY; SYSTEM; INJURY; TRACT; EAE;
D O I
10.1016/j.neulet.2011.03.021
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
In the present study, we demonstrate that the histopathologic features of myelin oligodendrocyte glycoprotein (MOG) peptide 35-55-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice closely mirror the hallmarks of MS pathology. On the one hand, we depict a time-dependent transition from acute inflammation to chronic neurodegeneration in spinal cord histopathology and provide distinct criteria (i.e. parenchymal edema, cellular infiltration and perivascular inflammatory infiltrates) by which acute and chronic stages of the disease can be distinguished. On the other hand, we assessed the extent of spinal cord plaque formation in relation to the total white matter area and we demonstrate a strong correlation with the clinical disease severity. Additionally, we report on the involvement of different spinal cord regions, focusing on the anterolateral, posterior and pyramidal tract. Our results help to further characterize histopathology of MOG peptide 35-55-induced EAE and reinforce the importance of this model for structural and functional studies of MS features. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:227 / 231
页数:5
相关论文
共 17 条
[1]
Motor neuron pathology in experimental autoimmune encephalomyelitis:: studies in THY1-YFP transgenic mice [J].
Bannerman, PG ;
Hahn, A ;
Ramirez, S ;
Morley, M ;
Bönnemann, C ;
Yu, S ;
Zhang, GX ;
Rostami, A ;
Pleasure, D .
BRAIN, 2005, 128 :1877-1886
[2]
Berger T, 1997, LAB INVEST, V76, P355
[3]
Myelin oligodendrocyte glycoprotein: A novel candidate autoantigen in multiple sclerosis [J].
Bernard, CCA ;
Johns, TG ;
Slavin, A ;
Ichikawa, M ;
Ewing, C ;
Liu, J ;
Bettadapura, J .
JOURNAL OF MOLECULAR MEDICINE-JMM, 1997, 75 (02) :77-88
[4]
Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE [J].
Craner, MJ ;
Hains, BC ;
Lo, AC ;
Black, JA ;
Waxman, SG .
BRAIN, 2004, 127 :294-303
[5]
Axonal damage correlates with disability in patients with relapsing-remitting multiple sclerosis - Results of a longitudinal magnetic resonance spectroscopy study [J].
De Stefano, N ;
Matthews, PM ;
Fu, LQ ;
Narayanan, S ;
Stanley, J ;
Francis, GS ;
Antel, JP ;
Arnold, DL .
BRAIN, 1998, 121 :1469-1477
[6]
Axonal damage in acute multiple sclerosis lesions [J].
Ferguson, B ;
Matyszak, MK ;
Esiri, MM ;
Perry, VH .
BRAIN, 1997, 120 :393-399
[7]
Goverman J, 1996, LAB ANIM SCI, V46, P482
[8]
Pattern of axonal injury in murine myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis: Implications for multiple sclerosis [J].
Herrero-Herranz, Eva ;
Pardo, Luis A. ;
Gold, Ralf ;
Linker, Ralf A. .
NEUROBIOLOGY OF DISEASE, 2008, 30 (02) :162-173
[9]
Targeting experimental autoimmune encephalomyelitis lesions to a predetermined axonal tract system allows for refined behavioral testing in an animal model of multiple sclerosis [J].
Kerschensteiner, M ;
Stadelmann, C ;
Buddeberg, BS ;
Merkler, D ;
Bareyre, FM ;
Anthony, DC ;
Linington, C ;
Brück, W ;
Schwab, ME .
AMERICAN JOURNAL OF PATHOLOGY, 2004, 164 (04) :1455-1469
[10]
Fundamental differences in the dynamics of CNS lesion development and composition in MP4-and MOG peptide 35-55-induced experimental autoimmune encephalomyelitis [J].
Kuerten, Stefanie ;
Javeri, Sita ;
Tary-Lehmann, Magdalena ;
Lehmann, Paul V. ;
Angelov, Doychin N. .
CLINICAL IMMUNOLOGY, 2008, 129 (02) :256-267