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由LPS诱导的细胞外AREG会通过EGFR/TLR4信号通路触发巨细胞的灭

Gang Yuan¹, Qudi Qiao¹, Aolin Jiang¹

¹Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.

Frontiers in immunology

|April 28, 2025

概括

细胞外安菲瑞古林 (AREG) 通过EGFR/TLR4信号传递驱动了败血性巨的热. 抑制AREG或其通路可能提供新的败血症治疗方法.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

恩菲瑞古林 (AREG) 是EGF家族的一种成员,是一种细胞外释放的跨膜蛋白.
细胞外AREG在败血性巨细胞灭中的作用尚不清楚.

研究的目的:

为了研究细胞外AREG在败血性巨细胞,小鼠和患者中的功能.

主要方法:

通过RPLP1.1.研究了细胞外AREG调节.
分析了细胞外AREG对细胞因子和热灭菌标记物表达的影响.
使用了AREG中和抗体,EGFR/NF-κB抑制剂和TLR4/Myd88淘汰模式.
评估了AREG在败血症小鼠模型和人类败血症患者中的作用.

主要成果:

高细胞外AREG表达,由RPLP1调节,促进IL-6,CCL2,CCL3,Caspase-1,IL-1β和Nlrp3的表达,诱导巨细胞质死.
细胞外AREG和ATP触发热;AREG中和减少了LPS诱导的EGFR激活,TLR4表达和热.
通过EGFR/NF-κB的抑制和TLR4/Myd88淘汰赛来减少热.
细胞外AREG会加剧小鼠的败血症,但通过DTT预处理减弱.
艾瑞格调解人类的败血症,在严重病例中,途径基因上调.

结论:

由LPS诱导的细胞外AREG通过EGFR/TLR4/Myd88/NF-κB通路加剧了巨细胞的烧灭.
细胞外AREG在动物模型和人类的败血症发病过程中起着重要作用.
准AREG介导的烧途径为败血症提供了潜在的治疗策略.

关键词:

在 EGFR/TLR4 中,氨基氨酸 (Amphiregulin) 是一种氨基氨酸.巨细胞是一个巨细胞.热致灭 (pyroptosis) 是一种致的过程.这是一种血症.

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