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Suppression of chronic experimental autoimmune neuritis by nasally administered recombinant rat interleukin‐6
Author(s) -
Georgia Deretzi,
Sygkliti-Henrietta Pelidou,
LiPing Zou,
C Quiding,
Eilhard Mix,
Michael Levi,
B. Wahren,
Jie Zhu
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00749.x
Subject(s) - medicine , neuritis , immunology , nasal administration , immune system , antibody , adjuvant , tumor necrosis factor alpha , surgery
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–Barré 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 μg/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‐α (TNF‐α) 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.