Nuclear factor kappa B inhibitor suppresses experimental autoimmune neuritis in mice via declining macrophages polarization to M1 type.
Donghui ShenFengna ChuYue LangChao ZhengChunrong LiKangding LiuJie ZhuPublished in: Clinical and experimental immunology (2021)
Guillain-Barré syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of the peripheral nervous system (PNS). Macrophages play a central role in its animal model, experimental autoimmune neuritis (EAN), which has been well accepted. Additionally, nuclear factor (NF)-κB inhibitors have been used to treat cancers and have shown beneficial effects. Here, we investigated the therapeutic effect of M2 macrophage and the NF-κB pathway's correlation with macrophage activation in EAN in C57BL/6 mice. We demonstrate 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 proinflammatory 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.
Keyphrases
- nuclear factor
- toll like receptor
- adipose tissue
- signaling pathway
- multiple sclerosis
- drug induced
- sleep quality
- poor prognosis
- high fat diet induced
- liver failure
- immune response
- intensive care unit
- case report
- risk assessment
- respiratory failure
- physical activity
- aortic dissection
- high resolution
- sickle cell disease