NF- κB inhibitor suppresses experimental autoimmune neuritis in mice via declining macrophages polarization to M1 type

Clin Exp Immunol. 2021 Jun 12. doi: 10.1111/cei.13637. Online ahead of print.ABSTRACTGuillain-Barre' syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of peripheral nervous system (PNS). Macrophages play a central role in its animal model, experimental autoimmune neuritis (EAN), which 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's correlation with macrophages activation in EAN in C57BL/6 mice. We demonstrated that M2 macrophage transfusion could 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.PMID:34118070 | DOI:10.1111/cei.13637

Source: Clinical and Developmental Immunology - June 12, 2021 Category: Allergy & Immunology Authors: Donghui Shen Fengna Chu Yue Lang Chao Zheng Chunrong Li Kangding Liu Jie Zhu Source Type: research