Evidence map›Paper›PMID 26829557›Full record

ArticlePLoS pathogens2016

IFNs Modify the Proteome of Legionella-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid.

Jan Naujoks, Christoph Tabeling, Brian D Dill, Christine Hoffmann, Andrew S Brown, Mareike Kunze, Stefan Kempa, Andrea Peter, Hans-Joachim Mollenkopf, Anca Dorhoi and 13 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 2 pooled it
23.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

153 citing papers in PubMed, 2 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026
    Review
  5. Review
  6. Itaconate modifications: Mechanisms and applications.Journal of intensive medicine · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
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  16. Article
  17. Article
  18. Pathogen adaptation to lung metabolites.Current opinion in microbiology · 2025
    Review
  19. Review
  20. ACOD1-mediated lysosomal membrane permeabilization contributes toProceedings of the National Academy of Sciences of the United States of America · 2025
    Article

93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 9 institutions in 4 countries.

Jan NaujoksDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Christoph TabelingDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Brian D DillMRC Protein Phosphorylation Unit, University of Dundee, Dundee, United Kingdom.
Christine HoffmannMax-von-Pettenkofer Institute, Ludwig Maximilian University, Munich, Germany.
Andrew S BrownThe Department of Biochemistry and Molecular Biology, The University of Melbourne, Melbourne, Australia.
Mareike KunzeDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Stefan KempaIntegrative Metabolomics and Proteomics, Institute of Medical Systems Biology/Max-Delbrueck Center for Molecular Medicine, Berlin, Germany.
Andrea PeterDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Hans-Joachim MollenkopfMax Planck Institute for Infection Biology, Berlin, Germany.
Anca DorhoiMax Planck Institute for Infection Biology, Berlin, Germany.
Olivia KershawDepartment of Veterinary Pathology, Free University Berlin, Berlin, Germany.
Achim D GruberDepartment of Veterinary Pathology, Free University Berlin, Berlin, Germany.
Leif E SanderDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Martin WitzenrathDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Susanne HeroldMedizinische Klinik II, University Giessen and Marburg Lung Center, Justus-Liebig-University Giessen, Giessen, Germany.
Andreas NerlichDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Andreas C HockeDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Ian van DrielThe Department of Biochemistry and Molecular Biology, The University of Melbourne, Melbourne, Australia.
Norbert SuttorpDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Sammy BedouiThe Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Australia.
Hubert HilbiMax-von-Pettenkofer Institute, Ludwig Maximilian University, Munich, Germany.
Matthias TrostMRC Protein Phosphorylation Unit, University of Dundee, Dundee, United Kingdom.
Bastian OpitzDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité University Medicine Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEUniversity of Melbourne · AUFreie Universität Berlin · DELudwig-Maximilians-Universität München · DEMax Planck Institute for Infection Biology · DEMax Delbrück Center · DEMRC Protein Phosphorylation and Ubiquitylation Unit · GBUniversity of Dundee · GBUniversity of Giessen · DE

Funding

Medical Research Council G1100713Medical Research Council MC_UP_A500_1020Medical Research Council MC_UU_12016/5
6 · The paper itself

Abstract

Macrophages can be niches for bacterial pathogens or antibacterial effector cells depending on the pathogen and signals from the immune system. Here we show that type I and II IFNs are master regulators of gene expression during Legionella pneumophila infection, and activators of an alveolar macrophage-intrinsic immune response that restricts bacterial growth during pneumonia. Quantitative mass spectrometry revealed that both IFNs substantially modify Legionella-containing vacuoles, and comparative analyses reveal distinct subsets of transcriptionally and spatially IFN-regulated proteins. Immune-responsive gene (IRG)1 is induced by IFNs in mitochondria that closely associate with Legionella-containing vacuoles, and mediates production of itaconic acid. This metabolite is bactericidal against intravacuolar L. pneumophila as well as extracellular multidrug-resistant Gram-positive and -negative bacteria. Our study explores the overall role IFNs play in inducing substantial remodeling of bacterial vacuoles and in stimulating production of IRG1-derived itaconic acid which targets intravacuolar pathogens. IRG1 or its product itaconic acid might be therapeutically targetable to fight intracellular and drug-resistant bacteria.

Indexed as

ProteomeAnimalsDisease Models, AnimalFemaleGene Expression RegulationGene OntologyHydro-LyasesImmunity, InnateInterferonsLegionella pneumophilaLegionnaires' DiseaseMacrophages, AlveolarMiceMice, Inbred C57BLMice, TransgenicMitochondriaAcod1 protein, mouseHydro-LyasesInterferonsitaconic acidProteomeReactive Oxygen SpeciesSuccinates

Identifiers

PMID26829557
PMCPMC4734697
OpenAlexW2270624586

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.