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Intranasal Administration of Recombinant Mouse Interleukin‐12 Increases Inflammation and Demyelination in Chronic Experimental Autoimmune Neuritis in Lewis Rats
Author(s) -
Sygkliti-Henrietta Pelidou,
Zou Zou,
Deretzi,
Nennesmo,
Hsi Hsien Wei,
Mix,
van der Meide,
Wanxue Zhu
Publication year - 2000
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2000.00636.x
Subject(s) - medicine , neuritis , nasal administration , proinflammatory cytokine , immunology , inflammation , adjuvant , pharmacology , surgery
To examine whether interleukin (IL)‐12 modulates ongoing chronic experimental autoimmune neuritis (EAN), we evaluated the effects of recombinant mouse IL‐12 (rmIL‐12) in Lewis rats with chronic EAN, induced by immunization with P0 peptide (180–199) plus complete Freund's adjuvant. Rats were treated intranasally with either 0.1 or 1 μg/rat/day rmIL‐12 for 6 days from the onset of clinical chronic EAN, on days 5–10 postimmunization (p.i.). Only high‐dose rmIL‐12 exacerbated chronic EAN. This clinical effect was associated with higher numbers of inflammatory cells and more severe demyelination in sciatic nerve sections on days 15 and 80 p.i. compared with low‐dose rmIL‐12‐treated rats and phosphate‐buffered saline (PBS)‐treated control rats. High‐dose rmIL‐12 increased significantly the lymph node mononuclear cell proliferation in response to P0 peptide 180–199 and IFN‐γ production in the sciatic nerves. These data indicate that intranasally administered IL‐12 acts as a proinflammatory cytokine in chronic EAN. Effective inhibition of IL‐12 in vivo could be considered for therapeutic use in chronic inflammatory demyelinating polyradiculoneuropathy.