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长期免疫重编程的古典单细胞与改变的本体生成介导增强肺损伤的败血症幸存者

Scott J Denstaedt¹, Breanna McBean^2,3, Alan P Boyle^2,3

¹Division of Pulmonary and Critical Care Medici006Ee, Department of Internal Medicine, University of Michigan. Ann Arbor, Michigan, USA.

bioRxiv : the preprint server for biology

|June 6, 2025

概括

败血症幸存者因重编程的单细胞而面临呼吸衰竭的风险增加. 这些免疫细胞因先前的败血症而改变,促进肺损伤和中性粒细胞活动,影响长期健康.

科学领域:

免疫学免疫学免疫学
肺部病理学肺部病理学
关键护理医学关键护理医学

背景情况:

败血症幸存者经常因呼吸衰竭而住院治疗.
将先前的败血症与增强的肺损伤联系在一起的机制尚不清楚.
经典单细胞在败血症后持续存在,并表现出较高的细胞因子反应.

研究的目的:

为了研究免疫系统在败血症后对单细胞的重编程.
为了确定变化的单细胞本体产生是否有助于增强肺损伤.
阐明单细胞在败血症引起的肺损伤中的作用.

主要方法:

采用了先前败血症的小鼠模型,其次是二次脂多糖化物挑战.
在毒症后的不同时间点使用单细胞枯竭和收养转移.
分析了JAK-STAT信号,AP-1结合和单细胞谱系的变化.
检查了人类败血症/肺炎幸存者的单细胞特征.

主要成果:

败血症后单细胞对于增强的LPS诱导的肺损伤是必要的和足够的.
这些单细胞促进了中性粒细胞的脱粒化.
以前的败血症改变了单细胞信号通路,并倾斜了朝着中性粒细胞类表型的血统.
人体败血症幸存者的单细胞预测了死亡率,并显示了类似于中性粒细胞的特征.

结论:

败血症将单细胞重新编程为一种促炎性表型.
骨髓祖先和单细胞倾向于与中性粒细胞类似的血统.
这种重编程导致中性粒细胞脱粒化和随后的肺损伤.

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