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巨细胞保护对外围神经病的感觉轴突损失

Sara Hakim^1,2, Aakanksha Jain², Stuart S Adamson³

¹Department of Neurobiology, Harvard Medical School, Boston, MA, USA.

|February 12, 2025

概括

在患有2型糖尿病的肥胖小鼠中,巨细胞保护神经不受损害. 阻断这些免疫细胞使神经病变恶化,表明免疫反应可以预防糖尿病神经疾病.

科学领域:

免疫学
神经科学
代谢疾病研究

背景情况:

糖尿病周围神经病变 (DPN) 是2型糖尿病的常见,使人衰弱的并发症,通常与肥胖,失脂症和高血糖症有关.
虽然已知DPN的代谢联系,但炎症在其发病过程中的作用仍未得到充分研究.
由高脂肪,高果糖饮食 (HFHFD) 引起的肥胖和糖尿病前代谢变化为研究早期DPN的模型.

研究的目的:

调查炎症的贡献,特别是巨细胞透,在肥胖,糖尿病前的小鼠模型中的外周神经病变.
在饮食引起的肥胖和糖尿病前期情况下,确定外围神经的早期免疫反应是否具有保护性或有害性.

主要方法:

使用高脂肪,高果糖饮食 (HFHFD) 的小鼠诱导肥胖和糖尿病前代谢变化.
通过行为测试 (热量过敏症) 和皮肤神经纤维密度的组织学分析来评估外围神经病变.
单细胞坐骨神经测序以识别透的免疫细胞及其基因表达特征.
基因和药物抑制CCR2信号以阻止巨细胞的招募;删除Lgals3基因.

主要成果:

食HFHD小鼠出现热性低痛症和皮肤神经纤维密度降低,这表明外围神经病变.
在可检测的轴突退化之前,单细胞测序显示了CCR2+巨细胞的显著透到坐骨神经中.
通过CCR2阻断或Lgals3删除抑制巨细胞的招募,加剧了热性缺血和加速的皮肤消皮.
招募的巨细胞表达的基因与神经损伤模型和神经退行相关的微质标志物相似,尽管没有初始的轴突损失.

结论:

在肥胖和糖尿病前的小鼠中, 巨细胞被引入外周神经, 这是一种神经保护机制,
通过招募的巨细胞表达的Galactin-3在这种神经保护中起着关键作用.
增强和维持这些早期的神经保护性免疫反应可能是减缓或预防糖尿病患者外围神经病变的治疗策略.

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