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以E-selectin为媒介的NLRP3炎症酶的快速激活调节S100A8/S100A9从中性粒细胞通过短暂的气体皮质D孔形成释放S100A8/S100A9

Monika Pruenster¹, Roland Immler¹, Jonas Roth¹

¹Walter Brendel Centre of Experimental Medicine, Biomedical Center, Institute of Cardiovascular Physiology and Pathophysiology, Ludwig-Maximilians-Universität München, Planegg-Martinsried, Germany.

Nature immunology

|October 31, 2023

概括

NLRP3炎症酶和气皮素D控制中性粒细胞释放S100A8/S100A9,这是一个关键的炎症媒介. 这个过程是快速的,可逆的,对于控制炎症而不会导致细胞死亡至关重要.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

S100A8 / S100A9 是一种由髓状细胞在炎症条件下释放的亲炎症媒介.
从中性粒细胞醇中释放S100A8/S100A9的确切机制尚未完全理解.

研究的目的:

阐明从中性粒细胞中引起的E-选择因子S100A8/S100A9释放背后的分子机制.
为了确定参与这种炎症介质释放的信号通路.

主要方法:

研究了对中性粒细胞的E-selectin参与.
利用技术研究NLRP3炎症酶激活,流和气皮D功能.
研究了布鲁顿氨酸激酶和K_V1.3通道的作用.

主要成果:

由E-选择素诱导的S100A8/S100A9释放取决于NLRP3炎症体.
通过布鲁顿的氨酸激酶,E-选择因触发NLRP3酸化,导致流和ASC寡合化.
气体皮质D形成了短暂的孔隙,促进S100A8 / S100A9释放,并激活ESCRT III膜修复,而不会导致细胞死亡.

结论:

NLRP3炎症酶和气皮素D形成了一个快速,可逆的系统,用于控制中性粒细胞S100A8/S100A9释放.
这种机制对于在各种疾病期间控制中性粒细胞的炎症反应至关重要.

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