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

Akiyuki Uzawa; Masahiro Mori; Hiroki Masuda; Mayumi Muto; Ryohei Ohtani; Shinji Aoyama; Kazuyuki Matsushita; Satoshi Kuwabara

doi:10.1177/13524585241254731

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

Mult Scler. 2024 May 23:13524585241254731. doi: 10.1177/13524585241254731. Online ahead of print.

Authors

Akiyuki Uzawa¹, Masahiro Mori¹, Hiroki Masuda¹, Mayumi Muto¹, Ryohei Ohtani¹, Shinji Aoyama¹, Kazuyuki Matsushita², Satoshi Kuwabara¹

Affiliations

¹ Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
² Department of Laboratory Medicine, Chiba University Hospital, Chiba, Japan.

PMID: 38783607
DOI: 10.1177/13524585241254731

Abstract

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.

Keywords: Myelin oligodendrocyte glycoprotein antibody–associated disease; central nervous system; demyelination; interleukin-6; neurological recovery.