ArticleNature metabolism2022
TFEB induces mitochondrial itaconate synthesis to suppress bacterial growth in macrophages.
Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 97 citations in OpenAlex.
- Itaconation and Succination as Metabolite-Derived Cysteine Modifications in Inflammatory Signalling: Biochemical Mechanisms, Chemoproteomic Mapping, and Therapeutic Opportunities.Cell biochemistry and biophysics · 2026Review
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Nanomaterial-driven spatiotemporal autophagy modulation: The dual-edged sword in precision cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Spatial architecture of immunometabolism: Mitochondrial‑organelle interfaces in immune signaling (Review).International journal of molecular medicine · 2026Review
- TFEB Antagonizes Cardiac Hypertrophy and Failure by Enhancing Lysosomal Capacity and Mitochondrial Function.Circulation research · 2026Article
- Offense and defense: itaconate mediates bidirectional immune regulation of host-bacteria interaction.Journal of biomedical science · 2026Review
- Lipocalin-2 Restores Mitochondrial and Antioxidant Adaptation in a Strain-Specific Manner During LPS Induced Sepsis.Journal of cellular physiology · 2026Article
- Role of itaconate in intestinal disease (Review).International journal of molecular medicine · 2026Review
- Connexin Regulation and Modulation of Neural Stem Cell Differentiation Induced by Cell-Permeable Itaconate.Journal of cellular physiology · 2026Article
- Lactobacillus johnsonii-derived extracellular vesicles modulate gut microbiota metabolites and macrophage-related immune responses against Salmonella Typhimurium infection.Veterinary research · 2026Article
- T6SS mutants exploit itaconate to support infection of phagocytes.bioRxiv : the preprint server for biology · 2026Article
- NRF2 activators and the inhibitor of nuclear export, selinexor, restrict coronaviruses by targeting a network involving ACE2, TMPRSS2, and XPO1 through an NRF2-independent mechanism.Communications biology · 2026Article
- PRRSV-2 impedes lysosomes from eliminating secondary infected bacteria.PLoS pathogens · 2026Article
- Glycolytic reprogramming and immune responses in macrophages: a crosstalk driven by bacterial infection.Frontiers in immunology · 2026Review
- Molecular strategies ofFrontiers in cellular and infection microbiology · 2026Review
- How do immunometabolites shape bacterial infections?PLoS biology · 2026Article
- Analysis of mRNA and miRNA expression in RAW 264.7 macrophages infected withFrontiers in veterinary science · 2026Article
- Immune evasion of multidrug-resistant bacteria: insights from lung innate immune cells and targeted therapies.Frontiers in cellular and infection microbiology · 2026Review
- Mitochondria-lysosome crosstalk in microbial infections.Science China. Life sciences · 2025Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
Abstract
Successful elimination of bacteria in phagocytes occurs in the phago-lysosomal system, but also depends on mitochondrial pathways. Yet, how these two organelle systems communicate is largely unknown. Here we identify the lysosomal biogenesis factor transcription factor EB (TFEB) as regulator for phago-lysosome-mitochondria crosstalk in macrophages. By combining cellular imaging and metabolic profiling, we find that TFEB activation, in response to bacterial stimuli, promotes the transcription of aconitate decarboxylase (Acod1, Irg1) and synthesis of its product itaconate, a mitochondrial metabolite with antimicrobial activity. Activation of the TFEB-Irg1-itaconate signalling axis reduces the survival of the intravacuolar pathogen Salmonella enterica serovar Typhimurium. TFEB-driven itaconate is subsequently transferred via the Irg1-Rab32-BLOC3 system into the Salmonella-containing vacuole, thereby exposing the pathogen to elevated itaconate levels. By activating itaconate production, TFEB selectively restricts proliferating Salmonella, a bacterial subpopulation that normally escapes macrophage control, which contrasts TFEB's role in autophagy-mediated pathogen degradation. Together, our data define a TFEB-driven metabolic pathway between phago-lysosomes and mitochondria that restrains Salmonella Typhimurium burden in macrophages in vitro and in vivo.
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