• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

脂肪在溶酶体中:结核分枝杆菌如何欺骗巨噬细胞储存脂质。

The fat is in the lysosome: how Mycobacterium tuberculosis tricks macrophages into storing lipids.

出版信息

J Clin Invest. 2023 Mar 15;133(6):e168366. doi: 10.1172/JCI168366.

DOI:10.1172/JCI168366
PMID:36919697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10014092/
Abstract

Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), infects primarily macrophages, causing them to differentiate into lipid-laden foamy macrophages that are a primary source of tissue destruction in patients with TB. In this issue of the JCI, Bedard et al. demonstrate that 1-tuberculosinyladenosine, a virulence factor produced by M. tuberculosis, caused lysosomal dysfunction associated with lipid storage in the phagolysosome of macrophages in a manner that mimicked lysosomal storage diseases. This work sheds light on how M. tuberculosis manipulates host lipid metabolism for its survival and opens avenues toward host-directed therapy against TB.

摘要

结核分枝杆菌是结核病(TB)的病原体,主要感染巨噬细胞,使其分化为富含脂质的泡沫巨噬细胞,这是结核病患者组织破坏的主要来源。在本期 JCI 中,Bedard 等人表明,结核分枝杆菌产生的毒力因子 1-结核分枝杆菌腺苷,以模拟溶酶体贮积病的方式导致溶酶体功能障碍,并伴有巨噬细胞吞噬溶酶体中的脂质贮积。这项工作揭示了结核分枝杆菌如何操纵宿主的脂质代谢以维持其生存,并为针对结核病的宿主导向治疗开辟了途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/724c/10014092/12ef5afdbdb2/jci-133-168366-g040.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/724c/10014092/12ef5afdbdb2/jci-133-168366-g040.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/724c/10014092/12ef5afdbdb2/jci-133-168366-g040.jpg

相似文献

1
The fat is in the lysosome: how Mycobacterium tuberculosis tricks macrophages into storing lipids.脂肪在溶酶体中:结核分枝杆菌如何欺骗巨噬细胞储存脂质。
J Clin Invest. 2023 Mar 15;133(6):e168366. doi: 10.1172/JCI168366.
2
A terpene nucleoside from M. tuberculosis induces lysosomal lipid storage in foamy macrophages.结核分枝杆菌萜核苷诱导泡沫巨噬细胞溶酶体脂质蓄积。
J Clin Invest. 2023 Mar 15;133(6):e161944. doi: 10.1172/JCI161944.
3
Oxidized low-density lipoprotein (oxLDL) supports Mycobacterium tuberculosis survival in macrophages by inducing lysosomal dysfunction.氧化型低密度脂蛋白 (oxLDL) 通过诱导溶酶体功能障碍来支持巨噬细胞中的结核分枝杆菌存活。
PLoS Pathog. 2019 Apr 18;15(4):e1007724. doi: 10.1371/journal.ppat.1007724. eCollection 2019 Apr.
4
Infection-Driven Foamy Macrophages and Their Implications in Tuberculosis Control as Targets for Host-Directed Therapy.感染驱动的泡沫状巨噬细胞及其作为宿主导向治疗靶点在结核病控制中的意义。
Front Immunol. 2020 May 12;11:910. doi: 10.3389/fimmu.2020.00910. eCollection 2020.
5
Mycobacterium tuberculosis Infection Manipulates the Glycosylation Machinery and the N-Glycoproteome of Human Macrophages and Their Microparticles.结核分枝杆菌感染会操纵人类巨噬细胞及其微粒的糖基化机制和 N-糖蛋白质组。
J Proteome Res. 2017 Jan 6;16(1):247-263. doi: 10.1021/acs.jproteome.6b00685. Epub 2016 Nov 4.
6
WNT6/ACC2-induced storage of triacylglycerols in macrophages is exploited by Mycobacterium tuberculosis.分枝杆菌利用 WNT6/ACC2 诱导的巨噬细胞三酰基甘油储存。
J Clin Invest. 2021 Aug 16;131(16). doi: 10.1172/JCI141833.
7
Differential recruitment of CD63 and Rab7-interacting-lysosomal-protein to phagosomes containing Mycobacterium tuberculosis in macrophages.在巨噬细胞中,CD63 和 Rab7-interacting-lysosomal-protein 被招募到含结核分枝杆菌的吞噬体上存在差异。
Microbiol Immunol. 2010 Mar;54(3):170-4. doi: 10.1111/j.1348-0421.2010.00199.x.
8
MiR-1178 regulates mycobacterial survival and inflammatory responses in Mycobacterium tuberculosis-infected macrophages partly via TLR4.miR-1178 通过 TLR4 部分调节结核分枝杆菌感染的巨噬细胞中的分枝杆菌存活和炎症反应。
J Cell Biochem. 2018 Sep;119(9):7449-7457. doi: 10.1002/jcb.27054. Epub 2018 May 21.
9
Not too fat to fight: The emerging role of macrophage fatty acid metabolism in immunity to Mycobacterium tuberculosis.不过胖就不能战斗:巨噬细胞脂肪酸代谢在抗结核分枝杆菌免疫中的新作用。
Immunol Rev. 2021 May;301(1):84-97. doi: 10.1111/imr.12952. Epub 2021 Feb 8.
10
Targeting Molecular Inflammatory Pathways in Granuloma as Host-Directed Therapies for Tuberculosis.针对肉芽肿中分子炎症途径的宿主导向疗法治疗结核病。
Front Immunol. 2021 Oct 20;12:733853. doi: 10.3389/fimmu.2021.733853. eCollection 2021.

引用本文的文献

1
Deciphering tuberculosis: lysosome-centric insights into pathogenesis and therapies.解读结核病:以溶酶体为中心对发病机制和治疗方法的见解
Front Cell Infect Microbiol. 2025 May 14;15:1582037. doi: 10.3389/fcimb.2025.1582037. eCollection 2025.
2
Identification and assessment of hub genes and miRNAs coregulatory associated with immune infiltrations and drug interactions in latent tuberculosis based on MicroarrayData analysis, molecular docking, and dynamic simulation.基于微阵列数据分析、分子对接和动态模拟,鉴定和评估潜伏性结核病中与免疫浸润和药物相互作用相关的核心基因和miRNA共调节因子。
Biochem Biophys Rep. 2025 Feb 16;41:101952. doi: 10.1016/j.bbrep.2025.101952. eCollection 2025 Mar.
3

本文引用的文献

1
A terpene nucleoside from M. tuberculosis induces lysosomal lipid storage in foamy macrophages.结核分枝杆菌萜核苷诱导泡沫巨噬细胞溶酶体脂质蓄积。
J Clin Invest. 2023 Mar 15;133(6):e161944. doi: 10.1172/JCI161944.
2
Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis.氧化磷酸化选择性地协调组织巨噬细胞的动态平衡。
Immunity. 2023 Mar 14;56(3):516-530.e9. doi: 10.1016/j.immuni.2023.01.011. Epub 2023 Feb 3.
3
CRISPR Interference Reveals That All--Retinoic Acid Promotes Macrophage Control of Mycobacterium tuberculosis by Limiting Bacterial Access to Cholesterol and Propionyl Coenzyme A.
Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism.
通过选择性靶向脂质代谢来革新针对结核分枝杆菌感染的控制策略。
Cell Mol Life Sci. 2023 Sep 14;80(10):291. doi: 10.1007/s00018-023-04914-5.
CRISPR 干扰揭示了全反式视黄酸通过限制细菌获得胆固醇和丙酰辅酶 A 来促进巨噬细胞对结核分枝杆菌的控制。
mBio. 2022 Feb 22;13(1):e0368321. doi: 10.1128/mbio.03683-21. Epub 2022 Jan 18.
4
GABARAP sequesters the FLCN-FNIP tumor suppressor complex to couple autophagy with lysosomal biogenesis.GABARAP隔离FLCN - FNIP肿瘤抑制复合物,以使自噬与溶酶体生物发生相偶联。
Sci Adv. 2021 Oct;7(40):eabj2485. doi: 10.1126/sciadv.abj2485. Epub 2021 Oct 1.
5
WNT6/ACC2-induced storage of triacylglycerols in macrophages is exploited by Mycobacterium tuberculosis.分枝杆菌利用 WNT6/ACC2 诱导的巨噬细胞三酰基甘油储存。
J Clin Invest. 2021 Aug 16;131(16). doi: 10.1172/JCI141833.
6
Mycobacterium tuberculosis releases an antacid that remodels phagosomes.结核分枝杆菌释放出一种抗酸剂,重塑吞噬体。
Nat Chem Biol. 2019 Sep;15(9):889-899. doi: 10.1038/s41589-019-0336-0. Epub 2019 Aug 19.
7
Subcellular antibiotic visualization reveals a dynamic drug reservoir in infected macrophages.亚细胞抗生素可视化揭示了感染巨噬细胞中的动态药物储库。
Science. 2019 Jun 28;364(6447):1279-1282. doi: 10.1126/science.aat9689. Epub 2019 Jun 27.
8
Storage lipid studies in tuberculosis reveal that foam cell biogenesis is disease-specific.结核脂质贮积研究表明泡沫细胞的发生具有疾病特异性。
PLoS Pathog. 2018 Aug 30;14(8):e1007223. doi: 10.1371/journal.ppat.1007223. eCollection 2018 Aug.
9
Growth of in vivo segregates with host macrophage metabolism and ontogeny.在体内, 的生长与宿主巨噬细胞代谢和个体发生分离。
J Exp Med. 2018 Apr 2;215(4):1135-1152. doi: 10.1084/jem.20172020. Epub 2018 Mar 2.
10
Lipid droplet formation in Mycobacterium tuberculosis infected macrophages requires IFN-γ/HIF-1α signaling and supports host defense.分枝杆菌感染的巨噬细胞中脂滴的形成需要 IFN-γ/HIF-1α 信号通路的作用,并支持宿主防御。
PLoS Pathog. 2018 Jan 25;14(1):e1006874. doi: 10.1371/journal.ppat.1006874. eCollection 2018 Jan.