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在患有遗传长链脂肪酸氧化障碍的患者中,单细胞和巨细胞的概况

Sanne G S Verberk¹, Nico Hahn², Daan Heister²

¹Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam Institute for Infection and Immunity, Cancer Centre Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands; Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.

Biochimica et biophysica acta. Molecular basis of disease

|September 22, 2024

概括

患有长链脂肪酸氧化 (lcFAO) 疾病的患者表现出单细胞反应的改变. 具体来说,IL-4诱导的标记物与lcFAO有关,但在这些免疫细胞中没有观察到主要的炎症或代谢缺陷.

科学领域:

免疫学免疫学免疫学
代谢障碍代谢障碍代谢障碍
细胞生物学细胞生物学

背景情况:

遗传的长链脂肪酸氧化 (lcFAO) 障碍存在多种症状,通常由炎症恶化.
单细胞和巨细胞是关键的免疫细胞,参与炎症,在激活时经历代谢变化.
lcFAO疾病对单细胞/巨细胞代谢和功能的影响尚不清楚.

研究的目的:

在患有 lcFAO 疾病的患者中研究单细胞和巨细胞的表型和功能.
探索 lcFAO 疾病对这些免疫细胞的炎症反应和细胞代谢的影响.
确定粮农组织与替代性巨细胞激活之间的关系.

主要方法:

在11名lcFAO患者和11名对照组中,循环单细胞的表型化和血细胞因子分析.
在巨细胞中通过siRNA介导的ACADVL (VLCAD) 敲除,以建模非常长链乙基-CoA脱酶障碍 (VLCADD).
对表面标记物 (CD206,CD62L,CD200R) 和对脂多糖 (LPS) 和IL-4的反应进行分析.

主要成果:

lcFAO患者表现出血IL-1β和IL-6的升高,单细胞上CD206和CD62L的增加.
siVLCAD巨体显示了改变IL-4诱导的替代激活,但完整的LPS反应和新陈代谢.
来自lcFAO患者的单细胞衍生巨细胞显示IL-4诱导标记物 (CD206,CD200R) 的升高,没有主要的代谢或LPS诱导的炎症变化.

结论:

在lcFAO患者中的单细胞和巨细胞没有显著的炎症或代谢缺陷.
由IL-4诱导的替代巨细胞激活标记与lcFAO相关.
这些发现突显了lcFAO和IL-4驱动的巨细胞两极分化之间的特定联系.

关键词:

脂肪酸氧化障碍脂肪酸氧化障碍免疫代谢过程中的免疫代谢.免疫型定型免疫型定型炎症炎症是一种炎症.巨细胞是一个巨细胞.

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