ArticleInternational immunology2019
Metabolic adaptation to glycolysis is a basic defense mechanism of macrophages for Mycobacterium tuberculosis infection.
Article in International immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Meta-analysis reveals a core iron-responsive gene signature in Mycobacterium tuberculosis linking siderophore biosynthesis, virulence, and metabolic adaptation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Pooled it
- Type 2 diabetes mellitus associated microRNAs in tuberculosis susceptibility: a systematic review and bioinformatic analysis.Frontiers in endocrinology · 2026Pooled it
- MicroRNA-1246 regulates macrophage lipid metabolism and is involved in resistance to human Mycobacterium tuberculosis infection.PLoS pathogens · 2026Article
- IL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1ɑ/glycolysis pathway.Respiratory research · 2026Article
- Metabolic reprogramming of macrophages during mycobacterial infection: a review of immunometabolic crosstalk and pathogen manipulation.Frontiers in cellular and infection microbiology · 2026Review
- Inflammasome Activation Differences Underpin DifferentMedComm · 2025Article
- Metabolic rewiring of isoniazid sensitivity inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mycobacterium bovis frd operon phase variation hijacks succinate signaling to drive immunometabolic rewiring and pathogenicity.Nature communications · 2025Article
- Metabolic Changes in Zebrafish Larvae Infected withMetabolites · 2025Article
- BCG-derived acellular membrane vesicles elicit antimycobacterial immunity and innate immune memory.Frontiers in immunology · 2025Article
- The Role of Mitochondrial Regulation in Macrophage Polarization: Implications for the Pathogenesis of Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Mitochondria-Targeted Biomaterials-Regulating Macrophage Polarization Opens New Perspectives for Disease Treatment.International journal of nanomedicine · 2025Review
- Imaging the Architecture of Granulomas Induced by Mycobacterium tuberculosis Infection with Single-molecule Fluorescence In Situ Hybridization.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Identification and role of differentially expressed genes/proteins between pulmonary tuberculosis patients and controls across lung tissues and blood samples.Immunity, inflammation and disease · 2024Article
- Macrophage polarization in rheumatoid arthritis: signaling pathways, metabolic reprogramming, and crosstalk with synovial fibroblasts.Frontiers in immunology · 2024Review
- NAD(H) homeostasis underlies host protection mediated by glycolytic myeloid cells in tuberculosis.Nature communications · 2023Article
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- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are major components of tuberculosis (TB) granulomas and are responsible for host defenses against the intracellular pathogen, Mycobacterium tuberculosis. We herein showed the strong expression of hypoxia-inducible factor-1α (HIF-1α) in TB granulomas and more rapid death of HIF-1α-conditional knockout mice than wild-type (WT) mice after M. tuberculosis infection. Although interferon-γ (IFN-γ) is a critical host-protective cytokine against intracellular pathogens, HIF-1-deficient macrophages permitted M. tuberculosis growth even after activation with IFN-γ. These results prompted us to investigate the role of HIF-1α in host defenses against infection. We found that the expression of lactate dehydrogenase-A (LDH-A) was controlled by HIF-1α in M. tuberculosis-infected macrophages IFN-γ independently. LDH-A is an enzyme that converts pyruvate to lactate and we found that the intracellular level of pyruvate in HIF-1α-deficient bone marrow-derived macrophages (BMDMs) was significantly higher than in WT BMDMs. Intracellular bacillus replication was enhanced by an increase in intracellular pyruvate concentrations, which were decreased by LDH-A. Mycobacteria in phagosomes took up exogenous pyruvate more efficiently than glucose, and used it as the feasible carbon source for intracellular growth. These results demonstrate that HIF-1α prevents the hijacking of pyruvate in macrophages, making it a fundamental host-protective mechanism against M. tuberculosis.
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