实验性自身免疫性脑脊髓炎
脑脊髓炎
多发性硬化
脾脏
髓鞘碱性蛋白
髓鞘少突胶质细胞糖蛋白
免疫学
CCR1
趋化因子
免疫系统
生物
趋化因子受体
髓鞘
中枢神经系统
内分泌学
作者
Mushtaq Ahmad Ansari,Ahmed Nadeem,Sabry M. Attia,Saleh A. Bakheet,Mudassar Shahid,Muneeb U. Rehman,Mohammed M. Alanazi,Abdullah S. Alhamed,Khalid E. Ibrahim,Norah A. Albekairi,Sheikh F. Ahmad
出处
期刊:Immunobiology
[Elsevier]
日期:2022-09-01
卷期号:227 (5): 152245-152245
被引量:3
标识
DOI:10.1016/j.imbio.2022.152245
摘要
Multiple sclerosis (MS), an immune-mediated and neurodegenerative disorder of the central nervous system (CNS), is characterized by infiltrating myelin-reactive T lymphocytes and demyelinating lesions. Experimental autoimmune encephalomyelitis (EAE) is a well-established animal model used to study MS. To explore the impact of chemokine receptor CCR1 blockade in EAE and the underlying mechanisms, we used CCR1 antagonist J-113863 in PLP139-151-induced EAE in SJL/J mice. Following EAE induction, mice were treated with J-113863 (10 mg/kg) daily from day 14 until day 25. We investigated the effect of J-113863 on expression levels of GM-CSF, IL-6, IL-10, IL-27 in CD4+ spleen cells, using flow cytometry. We also analyzed the effect of J-113863 on GM-CSF, IL-6, IL-10, IL-27 mRNA and protein expression levels using RT-PCR and Western blot analysis in brain tissues. J-113863 treatment decreased the populations of CD4+GM-CSF+ and CD4+IL-6+ cells and increased CD4+IL-27+ and CD4+IL-10+ cells in the spleen. J-113863 had a suppressive effect on the mRNA and protein expression levels of GM-CSF, and IL-6 in the brain tissue. On the other hand, J-113863 treatment increased the mRNA and protein expression of IL-10 and IL-27 in the brain tissue. Our results highlighted J-113863's potential role in suppressing pro-inflammatory expression and up-regulating anti-inflammatory mediators, which could represent a beneficial alternative approach to MS treatment.
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