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

Author

Listed:
  • Lise Lefèvre

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • Hélène Authier

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • Sokrates Stein

    (Metabolic Signaling, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne)

  • Clarisse Majorel

    (Université de Toulouse, UMR 152, UPS)

  • Bettina Couderc

    (EA4553 Individualisation des traitements des cancers ovariens et ORL, UPS)

  • Christophe Dardenne

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • Mohamad Ala Eddine

    (Université de Toulouse, UMR 152, UPS)

  • Etienne Meunier

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • José Bernad

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • Alexis Valentin

    (Université de Toulouse, UMR 152, UPS)

  • Bernard Pipy

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

  • Kristina Schoonjans

    (Metabolic Signaling, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne)

  • Agnès Coste

    (UMR MD3, EA2405 Polarisation des Macrophages et Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, UPS
    Université de Toulouse, UMR 152, UPS)

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.

Suggested Citation

  • Lise Lefèvre & Hélène Authier & Sokrates Stein & Clarisse Majorel & Bettina Couderc & Christophe Dardenne & Mohamad Ala Eddine & Etienne Meunier & José Bernad & Alexis Valentin & Bernard Pipy & Kristi, 2015. "LRH-1 mediates anti-inflammatory and antifungal phenotype of IL-13-activated macrophages through the PPARγ ligand synthesis," Nature Communications, Nature, vol. 6(1), pages 1-13, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7801
    DOI: 10.1038/ncomms7801
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