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T. pallidum通过通过hexokinase 2阻断微质中的自流来实现免疫逃避

Xiao-Tong Wang¹, Lin Xie², Yun-Ting Hu²

¹Center of Clinical Laboratory, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China; Department of Laboratory, Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Laboratory of Digestive Cancer, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.

Microbial pathogenesis

|December 11, 2024

概括

在神经中,Treponema pallidum通过扰乱糖解和自,损害了微质免疫清除. 这种细菌抑制了hexokinase 2 (HK2),阻碍了细菌的消除并促进了免疫逃避.

科学领域:

神经免疫学神经免疫学
细胞的新陈代谢
传染性疾病传染性疾病

背景情况:

由Treponema pallidum (T. pallidum) 引起的神经,涉及大脑炎症和免疫细胞功能受损.
中枢神经系统的免疫细胞微细胞对于神经炎症和病原体清除至关重要.
无法消除T. pallidum表明受损的微质免疫清除.

研究的目的:

研究T. pallidum如何影响微质免疫清除.
探索这种免疫逃避的潜在代谢机制.
确定糖解和自在T. pallidum微细胞感染中的作用.

主要方法:

用于代谢分析的RNA测序 (RNAseq) 和LC-MS代谢学.
XFe96海马测定以评估微质代谢活动.
西方涂抹,qPCR和免疫光检测自流和感染水平.

主要成果:

T. pallidum改变了甘油酶 (HK1,HK2,LDHA) 的表达,导致了代谢失调.
减少了基酸盐和酸盐,观察到乳酸盐的产量增加.
微质糖解,糖解储备和最大容量受损.
T. pallidum感染抑制了HK2的表达,通过影响LAMP2和自菌体-溶酶体融合来抑制自菌体.

结论:

T. pallidum 劫持了微质糖解,以逃避免疫清除.
由T. pallidum抑制HK2可以调节自并增强免疫逃避.
代谢重编程是T. pallidum在神经期间免疫逃脱的关键机制.

关键词:

自自是一种自的过程.葡萄糖溶解是什么? 葡萄糖溶解六甲基酶 2 基酶 2 微质细胞中的微质细胞它们中的一个是Treponema pallidum.

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