The chemokine MCP-1 and the dendritic and myeloid cells it attracts are increased in the mSOD1 mouse model of ALS

被引:153
作者
Henkel, JS
Beers, DR
Siklós, L
Appel, SH
机构
[1] Methodist Res Inst, Dept Neurol, Houston, TX 77030 USA
[2] Biol Res Ctr, Dept Biophys, H-6701 Szeged, Hungary
关键词
ALS; dendritic cells; MCP-1; microglia; motoneuron; mSOD1;
D O I
10.1016/j.mcn.2005.10.016
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We recently demonstrated increased dendritic cells (potent antigen-presenting cells) and MCP-1 (monocyte, T-cell, and dendritic cell attracting chemokine) levels in ALS spinal cord tissue. Additionally, we presented data suggesting that dendritic cells might be contributing to the pathogenesis. To determine whether MCP-1 and dendritic cells are present in the mSOD1 mouse and how early in the disease process they are involved, we examined mSOD1 and control spinal cord tissue at different ages using real-time RT-PCR and immunohistochemistry. Dendritic cells were present and transcripts elevated in mSOD1 spinal cord beginning at 110 days. MCP-1 mRNA and immunoreactivity were upregulated in mSOD1 neuronal and glial cells as early as 15 days, prior to any evidence of microglial activation. CD68(+) cells were present at 39 days of age. Although it is not clear if these responses are protective or injurious, the early increased MCP-1 expression and CD68(+) cell presence indicate early preexisting injury. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:427 / 437
页数:11
相关论文
共 80 条
[1]
Immune reactivity in a mouse model of familial ALS correlates with disease progression [J].
Alexianu, ME ;
Kozovska, M ;
Appel, SH .
NEUROLOGY, 2001, 57 (07) :1282-1289
[2]
Inducible nitric oxide synthase up-regulation in a transgenic mouse model of familial amyotrophic lateral sclerosis [J].
Almer, G ;
Vukosavic, S ;
Romero, N ;
Przedborski, S .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (06) :2415-2425
[3]
Increased levels of the pro-inflammatory prostaglandin PGE2 in CSF from ALS patients [J].
Almer, G ;
Teismann, P ;
Stevic, Z ;
Halaschek-Wiener, J ;
Deecke, L ;
Kostic, V ;
Przedborski, S .
NEUROLOGY, 2002, 58 (08) :1277-1279
[4]
Almer G, 2001, ANN NEUROL, V49, P176, DOI 10.1002/1531-8249(20010201)49:2<176::AID-ANA37>3.3.CO
[5]
2-O
[6]
A critical pole for p38 mitogen-activated protein kinase in the maturation of human blood-derived dendritic cells induced by lipopolysaccharide, TNF-α, and contact sensitizers [J].
Arrighi, JF ;
Rebsamen, M ;
Rousset, F ;
Kindler, V ;
Hauser, C .
JOURNAL OF IMMUNOLOGY, 2001, 166 (06) :3837-3845
[7]
Distinct signaling pathways for MCP-1-dependent integrin activation and chemotaxis [J].
Ashida, N ;
Arai, H ;
Yamasaki, M ;
Kita, T .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (19) :16555-16560
[8]
Serum-induced monocyte differentiation and monocyte chemotaxis are regulated by the p38 MAP kinase signal transduction pathway [J].
Ayala, JM ;
Goyal, S ;
Liverton, NJ ;
Claremon, DA ;
O'Keefe, SJ ;
Hanlon, WA .
JOURNAL OF LEUKOCYTE BIOLOGY, 2000, 67 (06) :869-875
[9]
Babcock AA, 2003, J NEUROSCI, V23, P7922
[10]
Autoimmunity through cytokine-induced dendritic cell activation [J].
Banchereau, J ;
Pascual, V ;
Palucka, AK .
IMMUNITY, 2004, 20 (05) :539-550