IP-10 and MCP-1 levels in CSF and serum from multiple sclerosis patients with different clinical subtypes of the disease

被引:91
作者
Scarpini, E [1 ]
Galimberti, D [1 ]
Baron, P [1 ]
Clerici, R [1 ]
Ronzoni, M [1 ]
Conti, G [1 ]
Scarlato, G [1 ]
机构
[1] Univ Milan, IRCCS Osped Maggiore Policlin, Dino Ferrari Ctr, Dept Neurol Sci, I-20122 Milan, Italy
关键词
multiple sclerosis; inflammation; cerebrospinal fluid; chemokines; IP-10; MCP-1;
D O I
10.1016/S0022-510X(01)00680-3
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Interferon-gamma-inducible Protein-10 (IP-10) and Monocyte Chemotactic Protein-1 (MCP-1) levels were measured by enzyme-linked immunosorbent assay (ELISA) in the CSF and in the serum from 74 patients affected by different clinical fortes of Multiple Sclerosis (MS), including 39 patients with Relapsing Remitting (RR) MS in an active phase, 14 patients in a stable phase of the disease, 12 patients with Secondary Progressive (SP) MS and 9 patients with Primary Progressive (PP) MS. IP-10 and MCP-1 levels were also determined in 19 subjects with no neurological diseases or major systemic disorders, 18 patients with non-inflammatory neurological diseases, as well as in 15 patients with other inflammatory neurological diseases. IP-10 levels were significantly elevated in CSF and serum from RR and SP, but not PP-MS patients. On the contrary. MCP-1 levels were decreased in CSF and serum of all MS patients. CSF concentrations of IP-10 and MCP-1 did not significantly correlate neither with each other, nor with CSF mononuclear cell count, albumin quotient or CSF IgG index. No correlation between disease duration, clinical course or EDSS score and chemokine levels was found. IP-10 and MCP-1 undergo modifications indifferent subtypes of the disease: IP-10 levels in CSF and serum samples are markedly increased when inflammation is prominent, and not in PP-MS patients, where inflammation is less evident. MCP-1 decrease in CSF and serum from MS patients could be related to the regulation of T-cell polarization. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:41 / 46
页数:6
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