Contributions of CSF interleukin-6 elevation to the pathogenesis of myelin oligodendrocyte glycoprotein antibody-associated disease

被引:4
作者
Uzawa, Akiyuki [1 ]
Mori, Masahiro [1 ]
Masuda, Hiroki [1 ]
Muto, Mayumi [1 ]
Ohtani, Ryohei [1 ]
Aoyama, Shinji [1 ]
Matsushita, Kazuyuki [2 ]
Kuwabara, Satoshi [1 ]
机构
[1] Chiba Univ, Grad Sch Med, Dept Neurol, 1-8-1 Inohana,Chuo Ku, Chiba, Chiba 2608670, Japan
[2] Chiba Univ Hosp, Dept Lab Med, Chiba, Japan
关键词
Myelin oligodendrocyte glycoprotein antibody-associated disease; demyelination; central nervous system; interleukin-6; neurological recovery;
D O I
10.1177/13524585241254731
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare neuroinflammatory disorder characterized by acute episodes of central nervous system (CNS) demyelination. Previous studies have reported elevated interleukin (IL)-6 in cerebrospinal fluid (CSF) of MOGAD patients.Objective: We examined if CSF IL-6 level increase is associated with clinical parameters in MOGAD.Methods: IL-6 levels were measured using 44 CSF samples during the acute phase and 6 samples during recovery from 34 MOGAD patients, as well as 65 CSF samples from 45 aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4Ab + NMOSD), 107 samples from 76 multiple sclerosis patients, and 45 samples from neurodegenerative disease patients. Associations between IL-6 levels and clinical parameters in MOGAD were also evaluated.Results: CSF IL-6 levels were significantly comparably elevated during acute-phase in MOGAD and AQP4Ab + NMOSD, but declined following the acute phase. Among MOGAD patients, CSF IL-6 level was significantly correlated with CSF cell count, greater in patients with brain lesions than spinal cord lesions, and higher in CSF than serum, suggesting that excessive IL-6 is produced predominantly in CNS. Neurological recovery was tended to be poorer in MOGAD patients with higher CSF IL-6 level.Conclusion: CSF IL-6 may play important roles in the pathogenesis of MOGAD, especially in CNS inflammation.
引用
收藏
页码:977 / 982
页数:6
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