Suppression of chronic experimental autoimmune neuritis by nasally administered recombinant rat interleukin-6

Experimental autoimmune neuritis (EAN) is a CD4(+) T-cell-mediated demyelin ating disease of the peripheral nervous system (PNS) and serves as experime ntal model for human immunedemyelinating neurophathies, especially the Guil lain-Barre syndrome. In this study, we examined the effect of recombinant r at interleukin-6 (rrIL-6) on chronic EAN in Lewis rats induced by immunizat ion with P2 peptide 57-81 and Freund's complete adjuvant (FCA). Nasal admin istration of rat rIL-6 (1 mu g/rat/day) beginning in the initial phase of E AN as a therapeutic agent, decreased the severity and the duration of clini cal EAN. Low-grade inflammation and suppression of regional demyelination w ithin the sciatic nerves were seen in rrIL-6-treated rats. Hyporesponsivene ss of lymph node T cells, down-regulation of serum tumour necrosis factor-a lpha (TNF-alpha) and increased levels of P2-specific immunoglobulin G1 (IgG 1) antibodies document that nasal administration of rrIL-6 was effective sy stemically. However, because of the non-specific nature of the treatment an d multiple effects of IL-6, more experience and great caution are needed, b efore nasal administration of IL-6 can be considered as a treatment of huma n autoimmune demyelinating neurophathies.