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

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.