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动脉样硬化恶化肝脏缺血/再输液损伤通过干扰素调节因子-1过度表达在小鼠模型中

Ryosuke Nakano¹, Ichiya Chogahara¹, Masahiro Ohira²

¹Department of Gastroenterological and Transplant Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Minami-ku, Hiroshima, Japan.

Transplantation proceedings

|March 3, 2024

概括

动脉样硬化会通过激活免疫细胞,加剧缺血/再输血后的肝损伤. 这项研究揭示了动脉样硬化反映肝内免疫力,通过IL-15和IRF-1通道增加肝损伤.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
心血管研究研究心血管研究

背景情况:

腹腔大动脉化 (AAC) 与心血管死亡率和肝细胞癌肝切除术后的不良结果有关.
动脉样硬化对全身炎症和对缺血/反损伤 (IRI) 的反应的影响尚不清楚.

研究的目的:

为了研究动脉样硬化如何影响肝脏免疫系统在温暖缺血/反损伤 (IRI) 期间.

主要方法:

动脉样硬化 (ApoE-/-) 和野生型 (WT) 的小鼠接受了70%的肝脏紧1小时,随后进行了6小时的再输血.
分析了肝损伤,免疫细胞表型和基因表达 (IL-15,IRF-1).

主要成果:

与WT小鼠相比,动脉样硬化小鼠的肝损伤明显更大 (AST/ALT升高,组织学损伤).
动脉样硬化小鼠中的肝 T 细胞和 NK 细胞表现出更炎症的表型.
在动脉样硬化小鼠肝脏中观察到IL-15和IRF-1的升级.

结论:

动脉样硬化通过调节肝脏免疫来加剧肝脏IRI.
与IRF-1相关的IL-15生产增加,激活肝脏NK和T细胞,在动脉样硬化条件下恶化肝脏损伤.

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