一种Pseudomonas aeruginosa的定数感应代谢物通过甲基化途径操纵巨细胞铁亡
Tianyuan Jia1,2,3, Fengming Li4, Tianzhen Li4
1National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China. jiatianyuan2021@163.com.
Nature communications
|November 13, 2025
概括
Pseudomonas aeruginosa 使用 Pseudomonas quinolone 信号 (PQS) 来触发巨细胞中的铁亡. 这涉及一个新的途径,其中PQS增强铁的吸收,促进细胞死亡和病原体的生存.
科学领域:
- 细胞生物学 细胞生物学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 铁,一种由铁和脂质过氧化驱动的细胞死亡形式,与疾病有关.
- 病原体可以操纵宿主铁亡,但机制往往是未知的.
- Pseudomonas aeruginosa 是一种机会性病原体,需要铁才能生病和生存.
研究的目的:
- 阐明 Pseudomonas aeruginosa 在宿主巨细胞中诱导铁亡的机制.
- 为了确定参与P. aeruginosa介导的铁灭的特定分子和途径.
主要方法:
- 采用了基于高分辨率质谱的细胞热转移测定 (MS-CETSA) 和热蛋白质组分析.
- 研究了 Pseudomonas quinolone 信号 (PQS),卡诺辛-N-甲基转移酶 (CNMT) 和转激素受体 1 (TFR1) 的作用.
主要成果:
- P. aeruginosa利用PQS通过CNMT-TFR1甲基化途径诱导巨细胞中的铁亡.
- PQS与CNMT结合增强了其甲基转移酶活性,导致TFR1在His35.5的甲基化.
- 这种甲基化增加了TFR1的表达,促进了铁的获取,促进了铁.
结论:
- P. aeruginosa使用一个独特的PQS-CNMT-TFR1轴来诱导宿主巨细胞铁亡.
- 这种机制涉及劫持宿主表观遗传机器,以获得病原体的优势.
- 这些发现揭示了一种新的细菌策略,与利用宿主细胞死亡的其他病原体不同.
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