Bowman–Birk inhibitor concentrate suppresses experimental autoimmune neuritis via shifting macrophages from M1 to M2 subtype

• Bowman–Birk inhibitor concentrate inhibited experimental autoimmune neuritis signs.
• Suppression of experimental autoimmune neuritis related to T cells insufficiency.
• The suppressed mechanism is associated with shifting macrophages from M1 to M2.

BackgroundIn the present study, we investigated the immuno-regulatory and therapeutic effects of Bowman–Birk inhibitor concentrate (BBIC) on experimental autoimmune neuritis (EAN), an animal model of Guillain–Barré syndrome (GBS) in human.MethodsEAN in Lewis rats induced by inoculation with peripheral nerve myelin P0 protein peptide 180-199 (P0 peptide) was treated with BBIC at two different therapeutic regimens.ResultsOur data indicated that the administration of BBIC daily orally effectively inhibited and ameliorated the clinical and pathological signs of EAN. The suppression of EAN was associated with an insufficiency of autoreactive T cells, as reflected by inhibited P0 peptide-specific mononuclear cell proliferation and decreased in CD4 and CD8 T cells infiltrating into the peripheral nervous system (PNS). BBIC might mediate its therapeutic effects by shifting macrophages from M1 to M2 subtype as evidenced by increasing Arg-1, CD206 and IL-10 and inhibiting IFN-γ, TNF-α, IL-12, iNOS and CD40 expressions on macrophages as well as enhancing anti-inflammatory cytokines IL-4 and IL-10 and decreasing inflammatory cytokines, IFN-γ, TNF-α and IL-17 in the PNS.ConclusionOur results suggest that BBIC may have therapeutic potential in human GBS and other autoimmune diseases in the future.