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流动诱导的切割应力奖励NLRP3通过Piezo1激活巨细胞中的炎症酶激活

Adam Fish¹, Ashish Kulkarni^1,2

¹Department of Chemical Engineering, University of Massachusetts, Amherst, Massachusetts 01003, United States.

ACS applied materials & interfaces

|January 19, 2024

概括

像剪切应力这样的机械力量可以使NLRP3炎症酶激活. 高剪切应力大小更有效地主导免疫细胞,影响炎症反应和疾病进展.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
机械生物学机械生物学

背景情况:

NLRP3炎症酶是先天免疫的关键,对病原体和损伤做出反应.
环境因素影响免疫细胞功能,但机械力效应的理解较少.
剪切应激在NLRP3炎症酶激活中的作用及其分子机制需要进一步研究.

研究的目的:

为了研究切割应力作为NLRP3炎症酶激活的原始信号.
为了确定不同剪切应力大小对炎症原始体的影响.
阐明将剪切应力与NLRP3炎症酶激活联系起来的分子通路.

主要方法:

将不朽化骨髓衍生巨细胞 (iBMDMs) 暴露在生理剪切压力下.
化学诱导的炎症酶激活在剪切后的应激暴露.
通过ASC-CFP斑点形成和IL-1β分泌量化炎酶激活.
使用NLRP3和caspase-1淘汰的IBMDMs.
使用定量聚合酶链反应 (qPCR) 和小分子抑制剂.

主要成果:

更高的剪切应力大小更有效地启动了iBMDMs用于NLRP3炎症酶激活.
剪切应力诱导的原始依赖于NLRP3和caspase-1.
机理学研究表明,剪切应力可以提高Piezo1,IKKβ和NLRP3的表达.
在高强度剪切应力原始化后,IL-1β分泌显著增加.

结论:

剪切应力作为NLRP3炎症酶激活的显著原始信号.
剪切应力的大小与炎症原始化的程度相关.
剪切应力通过对关键分子组件的上调调节NLRP3炎症酶激活,提供了对炎症疾病病原体的见解.

关键词:

在NLRP3中,NLRP3是NLRP3中的一个.一些炎症一些炎症巨细胞是什么?巨细胞是什么?皮埃佐1 一个1 剪切压力的压力

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