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细胞外酸化增加了巨细胞中NLRP3-介导的炎症体信号传递

Byeong Jun Chae^1,2, Kyung-Seo Lee^1,2, Inhwa Hwang^1,2

¹Department of Microbiology and Immunology, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul 03722, Korea.

|July 7, 2023

概括

炎症导致酸性环境,增强巨细胞炎症酶激活. 这一过程涉及化物细胞内通道蛋白1 (CLIC1) 并可能提供治疗点.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

炎症涉及宿主防御感染和伤害.
炎症会通过增加糖解和乳酸分泌导致细胞外酸化.
炎症组织中的免疫细胞面临着酸性微环境,但其对炎症体信号传递的影响尚不清楚.

研究的目的:

为了研究细胞外化在巨细胞中炎症体信号传递中的作用.
为了确定酸性条件是否调节含有3 (NLRP3) 炎症体的NLR家族pyrin域的激活.
探索亚cidosis介导的炎症酶激活背后的机制.

主要方法:

巨细胞和中性粒细胞暴露于酸性条件 (低pH值) 或生理pH值.
测量了卡斯帕酶-1处理,IL-1β分泌和NLRP3炎症酶组合.
评估了细胞内pH值和CLIC1转移到血的情况.

主要成果:

在酸性环境中的巨细胞显示了增强的caspase-1处理和IL-1β分泌.
酸性pH增加了宏细胞但不是中性粒细胞的NLRP3炎症酶组合.
酸化降低了细胞内pH值,并促进了CLIC1在巨细胞中的转位,但不是中性粒细胞.

结论:

细胞外酸性增强NLRP3炎症酶激活在巨细胞在一个CLIC1-依赖的方式.
CLIC1转位是酸性中介炎症酶增强的一个关键机制.
CLIC1代表了NLRP3炎症酶相关疾病的潜在治疗标.

关键词:

这是一种酸性化症.化通道的使用.在炎症中,一些细胞会发炎.炎症炎症是一种炎症.作为NLR家族,它含有pyrin域的3蛋白 (NLRP3)

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