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重组TSP53减轻了CLP诱导的败血症小鼠的炎症和血脑屏障破坏

Deng Zhezhi¹, Sun Zaiyuan², Lu Gengxin¹

¹Department of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]

|January 27, 2026

概括

再组合的Trichinella spiralis 53-kDa糖蛋白 (rTsP53) 在预防败血症相关脑病变 (SAE) 中显示出有前途. 在小鼠的预防性rTsP53治疗减少了大脑炎症和血脑屏障损伤,这表明SAE的潜在治疗应用.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

败血症相关脑病变 (SAE) 是败血症的一种神经并发症,缺乏有效的药理疗法.
关键的病理包括过度的微质激活和血脑屏障 (BBB) 的破坏.
之前的研究表明,复合的Trichinella spiralis 53-kDa糖蛋白 (rTsP53) 在败血症小鼠中调节肠内皮紧接点.

研究的目的:

研究rTsP53作为SAE预防剂的潜力.
在败血症模型中阐明rTsP53影响大脑炎症和BBB完整性的机制.

主要方法:

对SAE患者的脑脊液 (CSF) 进行炎症标志物分析.
利用结刺 (CLP) 鼠标模型来诱导败血症.
在接受rTsP53治疗和未接受治疗的败血症小鼠中评估了大脑细胞因子,BBB透性,紧结蛋白,微质激活和p65水平.

主要成果:

SAE患者的脑脊髓暴露了炎症因子升高和白细胞迁移通路的上调.
临床肺炎小鼠的脑部炎症增加,BBB透性,微质激活和p65水平增加.
预防性rTsP53治疗降低了促炎性细胞因子 (IL-6,IL-17A),降低了p65,增加了抗炎因素 (IL-4,IL-13),并减轻了BBB损伤.

结论:

在小鼠模型中,预防性rTsP53的使用有效地减轻了败血症引起的脑炎症和BBB干扰.
rTsP53调节微质反应,为SAE提供了潜在的治疗策略.
这些临床前发现支持对rTsP53进行进一步的SAE预防研究.

关键词:

这是一种Trichinella spiralis抗原.血脑屏障血脑屏障血脑屏障血脑屏障微质细胞中的微质细胞败血症相关的脑病变 - - 败血症相关的脑病变

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