Amelioration of experimental allergic neuritis by sodium fusidate (fusidin): suppression of IFN-gamma and TNF-alpha and enhancement of IL-10

J Autoimmun. 1999 Sep;13(2):187-95. doi: 10.1006/jaut.1999.0317.

Abstract

The immunomodulating antibiotic drug fusidic acid and its sodium salt sodium fusidate (fusidin) ameliorate several organ-specific immunoinflammatory diseases. Because preliminary observations suggest that fusidin may also exert a beneficial effect in Guillain-Barré syndrome (GBS), here we have studied the effects of fusidin on actively induced experimental autoimmune neuritis (EAN) in rats, a known animal model for GBS. Both prophylactic and therapeutic treatment with fusidin (4 mg/rat day ip) markedly ameliorated the clinical course of the disease compared to vehicle-treated animals. The beneficial effects were associated with profound modifications of the capacity of these rats to produce and release pro- and anti-inflammatory cytokines such as IFN-gamma, TNF-alpha and IL-10, which are important in regulating the development of EAN.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Fusidic Acid / therapeutic use*
  • Guillain-Barre Syndrome / drug therapy
  • Guillain-Barre Syndrome / immunology
  • Immunosuppressive Agents / therapeutic use*
  • Interferon-gamma / metabolism*
  • Interleukin-10 / metabolism*
  • Lymphocyte Activation / drug effects
  • Male
  • Neuritis, Autoimmune, Experimental / drug therapy*
  • Neuritis, Autoimmune, Experimental / immunology
  • Rats
  • Rats, Inbred Lew
  • Spleen / cytology
  • Spleen / drug effects
  • Transcription, Genetic / drug effects
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Immunosuppressive Agents
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Fusidic Acid
  • Interferon-gamma