克鲁佩尔样因子-4介导的巨细胞极化和表型转变驱动肠道纤维化在THP-1单细胞模型在体外

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Takuya Kanno¹, Takahito Katano^1,2, Takaya Shimura¹

¹Department of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.

Medicina (Kaunas, Lithuania)

|May 25, 2024

概括

克鲁佩尔样因子4 (KLF4) 影响巨细胞的行为和细胞因子的产生,影响肠道纤维化. 准KLF4可能为治疗炎症性肠病 (IBD) 中的纤维化提供新的策略.

科学领域:

胃肠道学和免疫学
分子生物学和细胞机制

背景情况:

生物疗法已经推进了炎症性肠病 (IBD) 治疗,但纤维化相关的狭窄仍然是一个临床挑战.
了解驱动肠道纤维化的分子机制对于开发新型治疗策略至关重要.

研究的目的:

研究克鲁佩尔样因子4 (KLF4) 在肠道纤维化中的作用.
探索KLF4,巨细胞极化,细胞因子表达和纤维化发育中的 stromal myofibroblasts之间的相互作用.
为了检查KLF4对人类小肠器官的影响.

主要方法:

利用THP-1单细胞模型来评估KLF4表达及其对巨细胞极化和细胞因子概况的影响.
进行了与树叶肌纤维细胞和条件化巨细胞介质的共同培养实验.
使用人类诱导的多能干细胞衍生的小肠器官来模拟体内反应.

主要成果:

不同的巨细胞亚型显示出不同的KLF4表达模式和功能.
KLF4倒置改变了细胞因子表达,M2b巨细胞通过IL-10显示了抗纤维效应.
巨细胞-肌纤维细胞相互作用促进了炎症表型和与纤维化相关的IL-36α的上调.

结论:

KLF4在调节巨细胞两极分化和调解肠纤维化至关重要的相互作用方面发挥着重要作用.
这项研究提供了关于纤维化病原体中细胞组件和细胞因子的复杂相互作用的见解.
这些发现表明,在IBD中减轻纤维化可能是治疗点.

关键词:

人类诱导的多能干细胞干细胞.炎症性肠病是一种炎症性肠病.互白素-1-1的使用情况.介质蛋白-10 介质蛋白-10 是一种介质蛋白-36 的作用.肌纤维母细胞细胞.

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