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在败血症休克中出现免疫代谢混乱

Deepmala Shrestha¹, Bishnu D Pant¹, Sanjoy Roychowdhury¹

¹Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195, United States.

Journal of leukocyte biology

|September 28, 2024

概括

败血性休克会导致由于代谢变化而导致免疫抑制. 感染性休克患者的血代谢物累积改变了免疫细胞的反应,导致内毒素耐受性和感染风险增加.

科学领域:

免疫学免疫学免疫学
代谢学代谢学代谢学
关键护理医学关键护理医学

背景情况:

败血性休克的死亡率很高,其特点是免疫系统的调节失调,从超炎症转变为低炎症.
低炎症增加了对二次感染的易感性,但血代谢产物在这个阶段的作用尚不清楚.
了解代谢变化对于管理败血症休克的免疫抑制至关重要.

研究的目的:

为了研究积累的血代谢物的免疫细胞功能的影响,在性休克的低炎症阶段.
为了确定特定的代谢物是否会影响周围血液单核细胞 (PBMCs) 的炎症反应.
为了确定与败血症休克中内毒素耐受性相关的代谢特征.

主要方法:

在全血中分析了TNF蛋白对脂聚糖化物 (LPS) 刺激的反应,来自败血症休克患者和健康对照组.
进行了血代谢分析,以确定在败血症休克中积累的代谢物.
在体外暴露健康对照PBMCs各种代谢物,并评估其LPS诱导的炎症反应.

主要成果:

败血性休克患者表现出内毒素耐受性,与高调节TNF蛋白的健康对照不同.
在败血性冲击等离子体中观察到碳水化合物,氨基酸,脂肪酸,胺,斯芬戈米林和TCA循环代谢物的显著积累.
在体外,一些代谢物被抑制,而另一些代谢物上调调节了PBMC对LPS的炎症反应.

结论:

在败血症休克中耐受性内毒素表型与广泛的血代谢物积累有关.
这些累积的代谢物显著调节循环免疫细胞的免疫反应.
代谢失调在性休克中所见的免疫抑制中起着根本性的作用,可能导致二次感染.

关键词:

代谢代谢代谢代谢单细胞 (Monocytes) 是一种单细胞.这是一种血症.败血症的冲击是一个令人震惊的现象.

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