Guillain–Barre’ syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of peripheral nervous system (PNS). Macrophages playing a central role in its animal model, experimental autoimmune neuritis (EAN) has been well-accepted. Additionally, NF-κB inhibitors has been used to treat cancers and showed beneficial effects. Here we investigated the therapeutic effect of M2 macrophage and NF-κB pathway is correlated with macrophages activation in experimental autoimmune neuritis (EAN) in C57BL/6 mice. We demonstrated that M2 macrophage transfusion can alleviate the clinical symptoms of EAN by reducing the proportion of M1 macrophage in the peak period, inhibiting the phosphorylation of NF-κB p65. The NF-κB inhibitor (BAY-11-7082) could alleviate the clinical symptoms of EAN and shorten the duration of symptoms by reducing the proportion of M1 macrophages and the expression of pro-inflammatory cytokines. Consequently, BAY-11-7082 exhibits strong potential as a therapeutic strategy for ameliorating EAN by influencing the balance of M1/M2 macrophages and inflammatory cytokines.

Objectives: The aims of the study were to further elucidate the roles of M1 and M2 macrophages in the pathogenesis of EAE and the effects of treatment with M2 macrophages that target certain pro-inflammatory cytokines and with immunomodulatory preparations that beneficially influence the disease course should be in focus of future therapeutic trials. Results: Enhanced the total number of macrophages at the onset of clinical signs in the EAE group, consistent with an increased proportion of M1 cells and low numbers of M2 cells. As the disease progressed and the symptoms worsened, M1 cells were decreased and M2 cells were gradually increased till the peak. In the recovery stage, M2 cell numbers were gradually decreased. Treatment with M2 macrophages inhibited the NF-κb pathway, alleviated the symptoms of EAE, reduced inflammatory cell infiltration and demyelination in the central nervous system, and decreased the numbers of macrophages in the spleens. BAY-11-7082, an NF-κb blocking agent, could reduce the total number of macrophages both in vivo and in vitro, effectively prevented the EAE development, and significantly inhibited the symptoms EAE in mice. Conclusions: Macrophages may play a crucial role in the pathogenesis of EAE, while M2 macrophages have anti-inflammatory effects. Transfer of M2 macrophages to EAE mice can block the NF-κb pathway successfully and relieve the EAE symptoms. Application of NF-κb blockers is useful in the prevention and treatment of EAE.