Tumor necrosis factor-α and its soluble receptors in plasma and cerebrospinal fluid of multiple sclerosis patients treated with methylprednisolone

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Abstract

Demyelination is the main pathoiogical feature of multiple sclerosis (MS), a chronic inflammatory disease of the central nervous system. Tumor necrosis factor-α (TNF-α) can cause myelin damage and contribute to MS pathogenesis. We measured plasma and cerebrospinal fluid (CSF) levels of TNF-α and its soluble receptors, TNF-sRp55 and TNF-sRp75, in 18 patients with active MS, and in neurological and healthy controls. The same determinations were repeated on plasma and on CSF samples that were collected after the MS patients had ended a six-day treatment with high-dose methylprednisolone (MP). Pre- and post-treatment plasma and CSF TNF-α levels, when detectable, and those of TNF-sRp75, did not vary, and were similar to those of controls. CSF TNF-sRp55 levels were higher in acute MS patients than in controls. Post-treatment CSF TNF-sRp55 levels were higher than in the active phase of the disease. The MS patients, who clinically improved, tended to have the highest CSF TKF-sRp55 levels. The increase was due to intrathecal TNF-sRp55 synthesis. Although it is involved in MS pathogenesis. TNF-α is not detectable in plasma or in CSF samples from MS patients in various phases of the disease. A better marker of disease activity seems to be CSF TNF-sRp55 levels. The increased CSF levels of TNF-sRp55 in response to MP circumstantially suggest that this receptor could partially account for the beneficial effects of MP in acute MS.

Original languageEnglish
Pages (from-to)431-436
Number of pages6
JournalEuropean Cytokine Network
Volume10
Issue number3
Publication statusPublished - 1999

Keywords

  • Cerebrospinal fluid
  • Methylprednisolone
  • Multiple sclerosis
  • Tnf soluble receptors
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

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