结核分枝杆菌调控宿主脂质代谢重编程的研究进展

doi:10.19982/j.issn.1000-6621.20260098

中国防痨杂志 ›› 2026, Vol. 48 ›› Issue (8): 1214-1219.doi: 10.19982/j.issn.1000-6621.20260098

结核分枝杆菌调控宿主脂质代谢重编程的研究进展

曾李娜¹^,², 李文思²^,³, 卢海林²^,³, 汪文斐², 陈心春³, 邓国防⁴(), 谢水祥¹()

¹ 赣南医科大学基础医学院, 赣州 341000
² 国家感染性疾病临床医学研究中心, 深圳 518000
³ 深圳大学医学部, 深圳 518000
⁴ 深圳市第三人民医院肺病二科, 深圳 518000

收稿日期:2026-02-25 出版日期:2026-08-01 发布日期:2026-07-30
通信作者: 邓国防,Email:jxxk1035@yeah.net;谢水祥,Email:xsxw2002@163.com
基金资助:
深圳市第三人民医院研究基金(G202205);深圳市第三人民医院研究基金(G2022003);深圳市第三人民医院研究基金(G2022155);深圳市第三人民医院研究基金(24250G1025)

Advances in Mycobacterium tuberculosis regulation of host lipid metabolism reprogramming

Zeng Lina¹^,², Li Wensi²^,³, Lu Hailin²^,³, Wang Wenfei², Chen Xinchun³, Deng Guofang⁴(), Xie Shuixiang¹()

¹ School of Basic Medicine, Gannan Medical University, Ganzhou 341000, China
² National Clinical Research Center for Infectious Diseases, Shenzhen 518000, China
³ Shenzhen University School of Medicine, Shenzhen 518000, China
⁴ Division Two of Pulmonary Diseases, The Third People’s Hospital of Shenzhen, Shenzhen 518000, China

Received:2026-02-25 Online:2026-08-01 Published:2026-07-30
Contact: Deng Guofang, Email: jxxk1035@yeah.net; Xie Shuixiang, Email: xsxw2002@163.com
Supported by:
Research Fund of The Third People’s Hospital of Shenzhen(G202205);Research Fund of The Third People’s Hospital of Shenzhen(G2022003);Research Fund of The Third People’s Hospital of Shenzhen(G2022155);Research Fund of The Third People’s Hospital of Shenzhen(24250G1025)

摘要/Abstract

摘要：

结核病是由结核分枝杆菌(Mycobacterium tuberculosis, MTB)感染引起的全球性重大传染病,其长期持留与免疫逃逸能力是引发慢性感染的核心原因。脂质代谢在宿主-病原体相互作用中居于枢纽地位:MTB不仅能够主动劫持宿主脂质作为营养来源,还能系统性地重编程宿主脂质代谢网络,进而逃避免疫清除并建立持续感染。深入理解MTB劫持与重编程宿主脂质代谢的分子机制,可以为开发靶向宿主脂质代谢的宿主导向治疗提供重要的理论依据与潜在靶点。本文系统总结了MTB劫持宿主脂质作为营养来源、调控宿主脂质代谢重编程以实现免疫逃逸的分子机制,并对该领域未来的研究方向与临床转化前景进行展望。

关键词: 分枝杆菌, 结核, 巨噬细胞, 脂质代谢, 宿主与病原体相互作用

Abstract:

Tuberculosis is a major global infectious disease caused by Mycobacterium tuberculosis (MTB). The pathogen’s ability to establish long-term persistence and evade host immunity is central to the development of chronic infection. Lipid metabolism plays a pivotal role in host-pathogen interactions: MTB not only actively hijacks host lipids as a nutrient source but also systematically reprograms the host lipid metabolic network to evade immune clearance and establish persistent infection. A deeper understanding of the molecular mechanisms by which MTB hijacks and reprograms host lipid metabolism provides important theoretical foundations and potential targets for the development of host-directed therapies focusing on host lipid metabolism. This review systematically summarizes the molecular mechanisms by which MTB hijacks host lipids as a nutrient source and reprograms host lipid metabolism to achieve immune evasion, and discusses future research directions and clinical translation prospects in this field.

Key words: Mycobacterium tuberculosis, Macrophages, Lipid metabolism, Host-pathogen interactions

中图分类号:

R378.91

曾李娜, 李文思, 卢海林, 汪文斐, 陈心春, 邓国防, 谢水祥. 结核分枝杆菌调控宿主脂质代谢重编程的研究进展[J]. 中国防痨杂志, 2026, 48(8): 1214-1219. doi: 10.19982/j.issn.1000-6621.20260098

Zeng Lina, Li Wensi, Lu Hailin, Wang Wenfei, Chen Xinchun, Deng Guofang, Xie Shuixiang. Advances in Mycobacterium tuberculosis regulation of host lipid metabolism reprogramming[J]. Chinese Journal of Antituberculosis, 2026, 48(8): 1214-1219. doi: 10.19982/j.issn.1000-6621.20260098

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结核分枝杆菌调控宿主脂质代谢重编程的研究进展

Advances in Mycobacterium tuberculosis regulation of host lipid metabolism reprogramming

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