Evidence map›Paper›PMID 25119038›Full record

ArticleNature2014

AhR sensing of bacterial pigments regulates antibacterial defence.

Pedro Moura-Alves, Kellen Faé, Erica Houthuys, Anca Dorhoi, Annika Kreuchwig, Jens Furkert, Nicola Barison, Anne Diehl, Antje Munder, Patricia Constant and 16 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed, 1 pooled it
14.4field-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

212 citing papers in PubMed, 1 synthesis or guideline pooled it, 362 citations in OpenAlex.

  1. Influence of Alcohol on the Intestinal Immune System.Alcohol research : current reviews · 2025
    Pooled it
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152 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 5 institutions in 1 country.

Pedro Moura-Alves1] Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany [2].
Kellen Faé1] Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany [2].
Erica Houthuys1] Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany [2].
Anca Dorhoi1] Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany [2].
Annika KreuchwigLeibniz Institute for Molecular Pharmacology (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Jens FurkertLeibniz Institute for Molecular Pharmacology (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Nicola BarisonMax Planck Institute for Infection Biology, Structural Systems Biology, Charitéplatz 1, 10117 Berlin, Germany.
Anne DiehlLeibniz Institute for Molecular Pharmacology (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Antje MunderClinical Research Group, Clinic for Pediatric Pneumology, Allergology and Neonatology, OE 6710, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany.
Patricia ConstantInstitute of Pharmacology and Structural Biology (IPBS), CNRS and University of Toulouse (Toulouse III), 205 Route de Narbonne, 31077, Toulouse cedex 04, Toulouse, France.
Tatsiana SkrahinaMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Ute Guhlich-BornhofMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Marion KlemmMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Anne-Britta KoehlerMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Silke BandermannMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Christian GoosmannMicroscopy Core Facility, Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Hans-Joachim MollenkopfMicroarray Core Facility, Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Robert HurwitzProtein Purification Core Facility, Max Planck Institute for Infection Biology, Charitéplatz 1, 10117 Berlin, Germany.
Volker BrinkmannMicroscopy Core Facility, Max Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Simon FillatreauGerman Rheumatism Research Centre Berlin (DRFZ), a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany.
Mamadou DaffeInstitute of Pharmacology and Structural Biology (IPBS), CNRS and University of Toulouse (Toulouse III), 205 Route de Narbonne, 31077, Toulouse cedex 04, Toulouse, France.
Burkhard TümmlerClinical Research Group, Clinic for Pediatric Pneumology, Allergology and Neonatology, OE 6710, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany.
Michael KolbeMax Planck Institute for Infection Biology, Structural Systems Biology, Charitéplatz 1, 10117 Berlin, Germany.
Hartmut OschkinatLeibniz Institute for Molecular Pharmacology (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Gerd KrauseLeibniz Institute for Molecular Pharmacology (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
Stefan H E KaufmannMax Planck Institute for Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany.
Max Planck Society · DELeibniz Association · DEMax Planck Institute for Infection Biology · DECharité - Universitätsmedizin Berlin · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a highly conserved ligand-dependent transcription factor that senses environmental toxins and endogenous ligands, thereby inducing detoxifying enzymes and modulating immune cell differentiation and responses. We hypothesized that AhR evolved to sense not only environmental pollutants but also microbial insults. We characterized bacterial pigmented virulence factors, namely the phenazines from Pseudomonas aeruginosa and the naphthoquinone phthiocol from Mycobacterium tuberculosis, as ligands of AhR. Upon ligand binding, AhR activation leads to virulence factor degradation and regulated cytokine and chemokine production. The relevance of AhR to host defence is underlined by heightened susceptibility of AhR-deficient mice to both P. aeruginosa and M. tuberculosis. Thus, we demonstrate that AhR senses distinct bacterial virulence factors and controls antibacterial responses, supporting a previously unidentified role for AhR as an intracellular pattern recognition receptor, and identify bacterial pigments as a new class of pathogen-associated molecular patterns.

Indexed as

AnimalsAnti-Bacterial AgentsBasic Helix-Loop-Helix ProteinsBone Marrow CellsCytokinesFeedback, PhysiologicalHumansLigandsMacrophage ActivationMiceMycobacterium tuberculosisPhenazinesPigments, BiologicalPseudomonas aeruginosaPseudomonas InfectionsPyocyanineAhr protein, mouseAnti-Bacterial AgentsBasic Helix-Loop-Helix ProteinsCytokinesLigandsPhenazinesPigments, BiologicalPyocyanineReceptors, Aryl HydrocarbonReceptors, Pattern RecognitionVirulence Factors

Identifiers

PMID25119038
OpenAlexW2087435147

What OpenQuestion holds

Textmetadata
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.