Evidence map›Paper›PMID 25873311›Full record

ArticleNature communications2015

LRH-1 mediates anti-inflammatory and antifungal phenotype of IL-13-activated macrophages through the PPARγ ligand synthesis.

Lise Lefèvre, Hélène Authier, Sokrates Stein, Clarisse Majorel, Bettina Couderc, Christophe Dardenne, Mohamad Ala Eddine, Etienne Meunier, José Bernad, Alexis Valentin and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

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  12. Oral Administration ofJournal of fungi (Basel, Switzerland) · 2021
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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

13 authors.

Lise Lefèvre1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Hélène Authier1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Sokrates SteinMetabolic Signaling, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne 1015, Switzerland.
Clarisse MajorelUniversité de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Bettina CoudercEA4553 Individualisation des traitements des cancers ovariens et ORL, UPS, Toulouse 31400, France.
Christophe Dardenne1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Mohamad Ala EddineUniversité de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Etienne Meunier1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
José Bernad1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Alexis ValentinUniversité de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Bernard Pipy1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.
Kristina SchoonjansMetabolic Signaling, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne 1015, Switzerland.
Agnès Coste1] UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS, Toulouse 31400, France [2] Université de Toulouse, UMR 152, UPS, Toulouse 31400, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver receptor homologue-1 (LRH-1) is a nuclear receptor involved in the repression of inflammatory processes in the hepatointestinal tract. Here we report that LRH-1 is expressed in macrophages and induced by the Th2 cytokine IL-13 via a mechanism involving STAT6. We show that loss-of-function of LRH-1 in macrophages impedes IL-13-induced macrophage polarization due to impaired generation of 15-HETE PPARγ ligands. The incapacity to generate 15-HETE metabolites is at least partially caused by the compromised regulation of CYP1A1 and CYP1B1. Mice with LRH-1-deficient macrophages are, furthermore, highly susceptible to gastrointestinal and systemic Candida albicans infection. Altogether, these results identify LRH-1 as a critical component of the anti-inflammatory and fungicidal response of alternatively activated macrophages that acts upstream from the IL-13-induced 15-HETE/PPARγ axis.

Indexed as

AnimalsBlotting, WesternCandida albicansCandidiasisChromatin ImmunoprecipitationCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1CytokinesEnzyme-Linked Immunosorbent AssayFlow CytometryGastroenteritisHumansHydroxyeicosatetraenoic AcidsInterleukin-13MacrophagesMacrophages, Peritoneal15-hydroxy-5,8,11,13-eicosatetraenoic acidCyp1b1 protein, mouseCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1CytokinesHydroxyeicosatetraenoic AcidsInterleukin-13NR5A2 protein, humanNr5a2 protein, mousePPAR gammaReceptors, Cytoplasmic and NuclearSTAT6 Transcription Factor

Identifiers

PMID25873311
PMCPMC4410638

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.