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

نویسندگان

  • Lise Lefèvre
  • Hélène Authier
  • Sokrates Stein
  • Clarisse Majorel
  • Bettina Couderc
  • Christophe Dardenne
  • Mohamad Ala Eddine
  • Etienne Meunier
  • José Bernad
  • Alexis Valentin
  • Bernard Pipy
  • Kristina Schoonjans
  • Agnès Coste
چکیده

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.

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عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015