实验性自身免疫脑膜炎的发病因子随着动物的年龄而改变:S100B表达的影响
Ana Rita Ribeiro1, Raquel Pereira1, Catarina Barros1
1Faculdade de Farmácia, Research Institute for Medicines (iMed.ULisboa), Universidade de Lisboa, Lisbon, Portugal.
概括
年龄加剧多发性硬化症 (MS) 的严重程度,S100B升高会使疾病恶化. 切除S100B可以减少各个年龄段的炎症和化,为MS提供潜在的治疗点.
科学领域:
- 神经免疫学 神经免疫学
- 衰老的研究研究.
- 结合蛋白质是一种结合的蛋白质.
背景情况:
- 多发性硬化症 (MS) 是年轻人残疾的主要原因.
- 中年人的晚发性多发性硬化症往往表现出较差的结果.
- 较高的S100B蛋白与MS有关,并且在动物模型中准它显示出治疗前景.
- 有限的研究存在于与年龄相关的MS病理和S100B在整个生命周期中的作用.
研究的目的:
- 研究年龄对小鼠实验性自身免疫脑炎 (EAE) 的影响.
- 为了确定S100B淘汰赛 (KO) 能否减轻不同年龄组的多发性硬化病原性.
- 分析EAE中的特定年龄的脱髓化,炎症和免疫反应.
主要方法:
- 在年轻 (3个月),年长 (6个月) 和中年 (12个月) 的C57BL/6小鼠中诱导EAE,包括S100BKO对应物.
- 在诱导后的23天内,对小鼠进行了监测.
- 使用免疫组织化学和qPCR分析了脊髓; 脊髓细胞的特征是免疫细胞形状.
主要成果:
- 中年 (12个月) 的小鼠表现出更严重的EAE过程,增加了结晶体,炎症和减少了微质细胞灭菌.
- 在所有年龄段的EAE小鼠中,S100B缺乏症降低了化和炎症标志物.
- 在12个月大的小鼠中,S100B KO导致调节性T细胞的增加.
结论:
- 衰老加剧了MS的发病过程,部分是由S100B的升高介导的.
- 在不同年龄段,S100B切除显示出对MS类病理的保护作用.
- 识别特定年龄的MS标志物和治疗点,如S100B,对于改善治疗结果至关重要.
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