Suppression of chronic experimental autoimmune neuritis by nasally administered recombinant rat interleukin-6
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Authors
Deretzi, G.
Pelidou, S.
Zou, L.
Quiding, C.
Mix, E.
Levi, M.
Wahren, B.
Zhu, J.
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peer-reviewed
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Immunology
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Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated demyelinating disease of the peripheral nervous system (PNS) and serves as experimental model for human immune-demyelinating neurophathies, especially the Guillain-Barre syndrome. In this study, we examined the effect of recombinant rat interleukin-6 (rrIL-6) on chronic EAN in Lewis rats induced by immunization with P2 peptide 57-81 and Freund's complete adjuvant (FCA). Nasal administration of rat rIL-6 (1 microg/rat/day) beginning in the initial phase of EAN as a therapeutic agent, decreased the severity and the duration of clinical EAN. Low-grade inflammation and suppression of regional demyelination within the sciatic nerves were seen in rrIL-6-treated rats. Hyporesponsiveness of lymph node T cells, down-regulation of serum tumour necrosis factor-alpha (TNF-alpha) and increased levels of P2-specific immunoglobulin G1 (IgG1) antibodies document that nasal administration of rrIL-6 was effective systemically. However, because of the non-specific nature of the treatment and multiple effects of IL-6, more experience and great caution are needed, before nasal administration of IL-6 can be considered as a treatment of human autoimmune demyelinating neurophathies.
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Keywords
Administration, Intranasal, Animals, Autoimmune Diseases/immunology/pathology/*therapy, Chronic Disease, Dose-Response Relationship, Immunologic, Immunoglobulin G/biosynthesis, Immunosuppression, Interleukin-6/*therapeutic use, Male, Neuritis, Autoimmune, Experimental/immunology/pathology/*therapy, Rats, Rats, Inbred Lew, Recombinant Proteins/therapeutic use, Sciatic Nerve/pathology, T-Lymphocyte Subsets/immunology, Tumor Necrosis Factor-alpha/metabolism
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http://www.ncbi.nlm.nih.gov/pubmed/10447716
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en
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Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής