Interleukin-6 levels in the cerebrospinal fluid and serum of patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Clinical and experimental findings suggest that humoral factors, such as anti-peripheral nerve antibodies and cytokines, may be implicated in the immunopathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Interleukin-6 (IL-6) is a multif...

Full description

Saved in:
Bibliographic Details
Published inJournal of neuroimmunology Vol. 47; no. 1; pp. 55 - 61
Main Authors Maimone, D., Annunziata, P., Simone, I.L., Livrea, P., Guazzi, G.C.
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 01.08.1993
Amsterdam Elsevier
New York, NY
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Clinical and experimental findings suggest that humoral factors, such as anti-peripheral nerve antibodies and cytokines, may be implicated in the immunopathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Interleukin-6 (IL-6) is a multifunctional cytokine that promotes immunoglobulin synthesis by B lymphocytes. Increased IL-6 release is associated with autoantibody production in a number of immune-mediated and neoplastic disorders. To investigate the possible involvement of abnormal IL-6 release in inflammatory polyneuropathies, we assayed IL-6 levels in the cerebrospinal fluid (CSF) and serum of 23 patients with acute GBS and seven with CIDP. We also studied 69 patients with other non-inflammatory neurological diseases (NIND), 25 with other inflammatory neurological diseases (IND), four with brain tumors (BT), and 15 normal donors (serum alone) as controls. We found detectable levels of IL-6 in the CSF of 57% of GBS, 43% of CIDP, 60% of IND, 75% of BT, and 4% of NIND. In GBS patients, no correlation was found between CSF IL-6 values and other laboratory or clinical parameters, such as CSF total protein, CSF albumin, CSF IgG, CSF/serum albumin ratio, functional disability score, and time elapsed from disease onset. Serum IL-6 levels were increased in six of 23 (26%) GBS, in one of 39 (3%) NIND, and in one of seven (14%) IND, but in none of the CIDP or BT patients. There was no correlation between serum and CSF IL-6 values, but cytokine levels in GBS sera correlated with time elapsed from clinical onset. In addition, we measured anti-GM1 IgG and IgM levels in the CSF and sera of GBS and CIDP patients to study the possible association of these autoantibodies with increased IL-6 secretion. In both CSF and sera of GBS or CIDP patients, increased anti-GM1 antibody levels were not associated with elevated IL-6. We conclude that elevated IL-6 levels are frequently detected in the CSF of patients with inflammatory polyneuropathies, especially GBS. The presence of a heightened IL-6 release, however, is not required for the production of anti-GM1 antibodies in GBS and CIDP patients. Additional studies may clarify whether testing CSF IL-6 levels in the early phase of GBS would help in defining the inflammatory nature of the polyneuropathy, prompting a faster choice of plasma exchange treatment.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0165-5728
1872-8421
DOI:10.1016/0165-5728(93)90284-6