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.
M1 Macrophage Derived Exosomes Aggravate Experimental Autoimmune Neuritis via Modulating Th1 Response