ArticlePLoS pathogens2021
Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Lipidomics of longer-term effects in the murine model after exposure to mixed field radiation and combined infection.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- In vivo dual RNA-Seq uncovers key effectors of epithelial barrier disruption by an extracellular pathogen.Nature communications · 2026Article
- Metabolically hijacked Listeria monocytogenes synergizes STING activation and dual cell death for enhanced antitumor immunotherapy.Journal of nanobiotechnology · 2025Article
- Dietary restriction reprograms CD8Nature metabolism · 2025Article
- Effects of Combined Bacterial Infection and Radiation Injury on Biofluid Metabolite Profiles in the Murine Model.ACS omega · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Listeria monocytogenes requires phosphotransferase systems to facilitate intracellular growth and virulence.PLoS pathogens · 2025Article
- Transcriptional control of metabolism by interferon regulatory factors.Nature reviews. Endocrinology · 2024Review
- Mitochondrial electron transport chain in macrophage reprogramming: Potential role in antibacterial immune response.Current research in immunology · 2024Review
- Ketolysis drives CD8Immunity · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Listeria monocytogenes (L. monocytogenes) is a food-borne bacterial pathogen. Innate immunity to L. monocytogenes is profoundly affected by type I interferons (IFN-I). Here we investigated host metabolism in L. monocytogenes-infected mice and its potential control by IFN-I. Accordingly, we used animals lacking either the IFN-I receptor (IFNAR) or IRF9, a subunit of ISGF3, the master regulator of IFN-I-induced genes. Transcriptomes and metabolite profiles showed that L. monocytogenes infection induces metabolic rewiring of the liver. This affects various metabolic pathways including fatty acid (FA) metabolism and oxidative phosphorylation and is partially dependent on IFN-I signaling. Livers and macrophages from Ifnar1-/- mice employ increased glutaminolysis in an IRF9-independent manner, possibly to readjust TCA metabolite levels due to reduced FA oxidation. Moreover, FA oxidation inhibition provides protection from L. monocytogenes infection, explaining part of the protection of Irf9-/- and Ifnar1-/- mice. Our findings define a role of IFN-I in metabolic regulation during L. monocytogenes infection. Metabolic differences between Irf9-/- and Ifnar1-/- mice may underlie the different susceptibility of these mice against lethal infection with L. monocytogenes.
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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.