ArticlePLoS pathogens2018
Lipid droplet formation in Mycobacterium tuberculosis infected macrophages requires IFN-γ/HIF-1α signaling and supports host defense.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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Who cites it
134 citing papers in PubMed, 215 citations in OpenAlex.
- Monocyte metabolic transcriptional programs associate with resistance to tuberculin skin test/interferon-γ release assay conversion.The Journal of clinical investigation · 2021Trial
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- MicroRNA-1246 regulates macrophage lipid metabolism and is involved in resistance to human Mycobacterium tuberculosis infection.PLoS pathogens · 2026Article
- Dopamine alters macrophage metabolism promoting intracellular Mycobacterium tuberculosis survival.Molecular medicine (Cambridge, Mass.) · 2026Article
- Antigen presentation by CD40Nature · 2026Article
- Potato purple top phytoplasma infection induces autophagy-associated lipid dynamics that support pathogen proliferation.Plant physiology · 2026Article
- PPE57 Cooperates with MmpL3 to Mediate Bacterial Lipid Transport and Promote Persistent Infection ofMicroorganisms · 2026Article
- Identification of a spatially organized TREM2-associated permissive macrophage niche in human pulmonary tuberculosis alveolar pneumonia.Nature communications · 2026Article
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- Lipid accumulation in tuberculosis granulomas inhibits macrophage-CD4Nature microbiology · 2026Article
- IL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1ɑ/glycolysis pathway.Respiratory research · 2026Article
- Obesity supersizes macrophage and neutrophil activation after stroke while lipid droplets play a protective role.Journal of neuroinflammation · 2026Article
- Low-density lipoprotein cholesterol drives multinucleated giant cell formation in response to mycobacterium bovis Bacille Calmette-Guérin.Scientific reports · 2026Article
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
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- Essential redundancies fuel Mycobacterium tuberculosis adaptation to the host.PLoS pathogens · 2025Review
- Systems analysis reveals alternate metabolic states adopted bybioRxiv : the preprint server for biology · 2025Article
- Kupyaphores─Self-Assembling Diisocyanolipopeptide ZnJournal of the American Chemical Society · 2025Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Lipid droplet (LD) formation occurs during infection of macrophages with numerous intracellular pathogens, including Mycobacterium tuberculosis. It is believed that M. tuberculosis and other bacteria specifically provoke LD formation as a pathogenic strategy in order to create a depot of host lipids for use as a carbon source to fuel intracellular growth. Here we show that LD formation is not a bacterially driven process during M. tuberculosis infection, but rather occurs as a result of immune activation of macrophages as part of a host defense mechanism. We show that an IFN-γ driven, HIF-1α dependent signaling pathway, previously implicated in host defense, redistributes macrophage lipids into LDs. Furthermore, we show that M. tuberculosis is able to acquire host lipids in the absence of LDs, but not in the presence of IFN-γ induced LDs. This result uncouples macrophage LD formation from bacterial acquisition of host lipids. In addition, we show that IFN-γ driven LD formation supports the production of host protective eicosanoids including PGE2 and LXB4. Finally, we demonstrate that HIF-1α and its target gene Hig2 are required for the majority of LD formation in the lungs of mice infected with M. tuberculosis, thus demonstrating that immune activation provides the primary stimulus for LD formation in vivo. Taken together our data demonstrate that macrophage LD formation is a host-driven component of the adaptive immune response to M. tuberculosis, and suggest that macrophage LDs are not an important source of nutrients for M. tuberculosis.
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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.