ArticleThe Journal of clinical investigation2023
A terpene nucleoside from M. tuberculosis induces lysosomal lipid storage in foamy macrophages.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- [Active Oxygen Influences Foam Macrophage Formation by Regulating Peroxisome Proliferator-Activated Receptor-γ Expression].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- Mycobacterium tuberculosis long-chain fatty acid resistome reveals universal stress protein TB15.3 as essential for infection.Communications biology · 2026Article
- CRISPRi-mediated silencing of the ABC transporterFrontiers in microbiology · 2026Article
- Lipid metabolism in the resuscitation of dormant mycobacterium tuberculosis: molecular resilience, host hijacking, and clinical opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Immunotherapy for tuberculosis: current strategies and future directions.Military Medical Research · 2025Review
- Cytidine diphosphate diacylglycerol synthase 2 is a synthetic lethal target in mesenchymal-like cancers.Nature genetics · 2025Article
- Deciphering tuberculosis: lysosome-centric insights into pathogenesis and therapies.Frontiers in cellular and infection microbiology · 2025Review
- LC-MS-based quantitation of proteomic changes induced by Norcantharidin in MTB-Treated macrophages.Proteome science · 2024Article
- Paired analysis of host and pathogen genomes identifies determinants of human tuberculosis.Nature communications · 2024Article
- Mycobacteria that cause tuberculosis have retained ancestrally acquired genes for the biosynthesis of chemically diverse terpene nucleosides.PLoS biology · 2024Article
- Article
- Exploring host-pathogen interactions in the Dictyostelium discoideum-Mycobacterium marinum infection model of tuberculosis.Disease models & mechanisms · 2024Review
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- Lipid droplets in pathogen infection and host immunity.Acta pharmacologica Sinica · 2024Review
- Cigarette Smoking as a Risk Factor for Tuberculosis in Adults: Epidemiology and Aspects of Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2024Review
- BBQ methods: streamlined workflows for bacterial burden quantification in infected cells by confocal microscopy.Biology open · 2024Article
- Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism.Cellular and molecular life sciences : CMLS · 2023Review
- The fat is in the lysosome: how Mycobacterium tuberculosis tricks macrophages into storing lipids.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
23 authors at 8 institutions in 6 countries.
Funding
Abstract
Induction of lipid-laden foamy macrophages is a cellular hallmark of tuberculosis (TB) disease, which involves the transformation of infected phagolysosomes from a site of killing into a nutrient-rich replicative niche. Here, we show that a terpenyl nucleoside shed from Mycobacterium tuberculosis, 1-tuberculosinyladenosine (1-TbAd), caused lysosomal maturation arrest and autophagy blockade, leading to lipid storage in M1 macrophages. Pure 1-TbAd, or infection with terpenyl nucleoside-producing M. tuberculosis, caused intralysosomal and peribacillary lipid storage patterns that matched both the molecules and subcellular locations known in foamy macrophages. Lipidomics showed that 1-TbAd induced storage of triacylglycerides and cholesterylesters and that 1-TbAd increased M. tuberculosis growth under conditions of restricted lipid access in macrophages. Furthermore, lipidomics identified 1-TbAd-induced lipid substrates that define Gaucher's disease, Wolman's disease, and other inborn lysosomal storage diseases. These data identify genetic and molecular causes of M. tuberculosis-induced lysosomal failure, leading to successful testing of an agonist of TRPML1 calcium channels that reverses lipid storage in cells. These data establish the host-directed cellular functions of an orphan effector molecule that promotes survival in macrophages, providing both an upstream cause and detailed picture of lysosome failure in foamy macrophages.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.