鲍曼-伯克抑制剂浓缩物通过将巨噬细胞从M1亚型转变为M2亚型来抑制实验性自身免疫性神经炎。
Bowman-Birk inhibitor concentrate suppresses experimental autoimmune neuritis via shifting macrophages from M1 to M2 subtype.
作者信息
Jin Tao, Yu Hong, Wang Dan, Zhang Hongliang, Zhang Bo, Quezada Hernan Concha, Zhu Jie, Zhu Wei
机构信息
Department of Neurology, the First Hospital, Jilin University, Xinmin Street 71#, 130021 Changchun, China.
Department of Otorhinolaryngology, Head and Neck Surgery, the First Hospital, Jilin University, Xinmin Street 71#, 130021 Changchun, China; Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital Huddinge, Hälsovägen 7, SE-141 86 Stockholm, Sweden.
出版信息
Immunol Lett. 2016 Mar;171:15-25. doi: 10.1016/j.imlet.2016.01.004. Epub 2016 Jan 11.
BACKGROUND
In the present study, we investigated the immuno-regulatory and therapeutic effects of Bowman-Birk inhibitor concentrate (BBIC) on experimental autoimmune neuritis (EAN), an animal model of Guillain-Barré syndrome (GBS) in human.
METHODS
EAN in Lewis rats induced by inoculation with peripheral nerve myelin P0 protein peptide 180-199 (P0 peptide) was treated with BBIC at two different therapeutic regimens.
RESULTS
Our data indicated that the administration of BBIC daily orally effectively inhibited and ameliorated the clinical and pathological signs of EAN. The suppression of EAN was associated with an insufficiency of autoreactive T cells, as reflected by inhibited P0 peptide-specific mononuclear cell proliferation and decreased in CD4 and CD8T cells infiltrating into the peripheral nervous system (PNS). BBIC might mediate its therapeutic effects by shifting macrophages from M1 to M2 subtype as evidenced by increasing Arg-1, CD206 and IL-10 and inhibiting IFN-γ, TNF-α, IL-12, iNOS and CD40 expressions on macrophages as well as enhancing anti-inflammatory cytokines IL-4 and IL-10 and decreasing inflammatory cytokines, IFN-γ, TNF-α and IL-17 in the PNS.
CONCLUSION
Our results suggest that BBIC may have therapeutic potential in human GBS and other autoimmune diseases in the future.
背景
在本研究中，我们研究了鲍曼-伯克抑制剂浓缩物（BBIC）对实验性自身免疫性神经炎（EAN）的免疫调节和治疗作用，EAN是人类吉兰-巴雷综合征（GBS）的动物模型。
方法
用外周神经髓鞘P0蛋白肽180-199（P0肽）接种诱导Lewis大鼠发生EAN，并采用两种不同的治疗方案用BBIC进行治疗。
结果
我们的数据表明，每日口服BBIC可有效抑制和改善EAN的临床和病理体征。EAN的抑制与自身反应性T细胞不足有关，这表现为P0肽特异性单核细胞增殖受到抑制以及浸润到外周神经系统（PNS）中的CD4和CD8 T细胞减少。BBIC可能通过将巨噬细胞从M1亚型转变为M2亚型来介导其治疗作用，这表现为巨噬细胞上的精氨酸酶-1（Arg-1）、CD206和白细胞介素-10（IL-10）增加，干扰素-γ（IFN-γ）、肿瘤坏死因子-α（TNF-α）、白细胞介素-12（IL-12）、诱导型一氧化氮合酶（iNOS）和CD40表达受到抑制，以及PNS中抗炎细胞因子IL-4和IL-10增加，炎性细胞因子IFN-γ、TNF-α和白细胞介素-17（IL-17）减少。
结论
我们的结果表明，BBIC未来可能对人类GBS和其他自身免疫性疾病具有治疗潜力。
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