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在Treponema Pallidum中,TP47蛋白通过PKM2-介导的代谢重编程触发巨细胞的炎症衰老

Jia-Wen Xie¹, Yin-Feng Guo¹, Shu-Hao Fan¹

¹Center of Clinical Laboratory, Zhongshan Hospital Xiamen University, School of Medicine, Xiamen University, Xiamen, China; Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.

International journal of biological macromolecules

|November 24, 2024

概括

它们中的一个是Treponema pallidum.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
细胞生物学细胞生物学

背景情况:

尽管巨细胞活动,但Treponema pallidum (T. pallidum) 的梅毒持续性尚不清楚.
细胞衰老,特别是炎症衰老诱导热,与宿主易感性有关.
代谢重编程在梅毒相关炎症衰老中的作用需要澄清.

研究的目的:

研究T. pallidum蛋白Tp47诱导巨细胞代谢重编程和炎症衰老的机制.
阐明Tp47介导的巨细胞功能障碍所涉及的分子相互作用和途径.

主要方法:

研究了Tp47对NLRP3炎症酶激活,热和巨细胞炎症衰老的作用.
使用生物化学分析分析了TP47,酸盐激酶M2 (PKM2) 和STUB1之间的相互作用.
评估了Tp47对PKM2酸化,代谢重编程和乳酸生产的影响.
评估了针对关键分子 (EIF2AK2,乳酸盐,糖解,PKM2) 的抑制剂在抑制Tp47诱导的衰老中的有效性.

主要成果:

Tp47通过EIF2AK2酸化激活了NLRP3炎酶介导的烧,导致炎症衰老和促炎细胞因子的释放.
Tp47通过与STUB1.1竞争性结合PKM2来抑制PKM2的无处不在和降解.
Tp47促进了PKM2 Y105酸化,推动了新陈代谢重编程,乳酸生产和随后的EIF2AK2酸化.
向抑制EIF2AK2,乳酸,糖解或PKM2有效降低了Tp47诱导的炎症衰老.

结论:

Tp47通过与PKM2相互作用来调节免疫代谢重编程,从而触发巨细胞中的炎症衰老.
这种相互作用代表了T. pallidum持久性和病变发生的新机制.
针对已识别的途径 (EIF2AK2,PKM2,代谢重编程) 为梅毒提供了潜在的治疗策略.

关键词:

炎症衰老是一种炎症性衰老.代谢重编程是一种代谢重编程.梅毒是什么梅毒是什么梅毒是什么

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