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PPAR-γ agonists, mainly 15d-PGJ(2), reduce eosinophil recruitment following allergen challenge

Thais S Farnesi-de-Assunção1, Claudiney F Alves, Vanessa Carregaro

  • 1Laboratory of Immunology, Federal University of Triangulo Mineiro, Uberaba, MG, Brazil.

Cellular Immunology
|December 24, 2011
PubMed

Insights

Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists like 15d-PGJ(2) effectively treat chronic eosinophilia by reducing eosinophil migration and production. These agonists modulate key cytokines, offering a novel therapeutic approach for eosinophil-driven diseases.

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Chronic eosinophilia involves excessive eosinophil accumulation, contributing to various inflammatory diseases.
  • Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor with known immunomodulatory functions.
  • Understanding PPAR-γ agonist effects on eosinophil-related pathways is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the immunomodulatory effects of PPAR-γ agonists 15d-PGJ(2) and rosiglitazone (RGZ) in a model of chronic eosinophilia.
  • To elucidate the specific mechanisms underlying the therapeutic potential of these agonists.

Main Methods:

  • Evaluation of eosinophil migration and eosinopoiesis in a chronic eosinophilia model.
  • Measurement of cytokine synthesis (IL-5, IL-33, IL-17, IL-23) and IgE levels following agonist treatment.
  • Assessment of eosinophilic response in IL-17 knockout mice.

Main Results:

  • 15d-PGJ(2) and RGZ significantly inhibited eosinophil migration and eosinopoiesis.
  • Treatment decreased Interleukin-5 (IL-5) synthesis, correlating with reduced eosinophil migration.
  • 15d-PGJ(2) reduced IgE levels, partly via B-cell inhibition, and both agonists decreased IL-33, IL-17, and IL-23 synthesis.
  • IL-17 knockout mice exhibited a blunted eosinophilic response, highlighting the role of IL-17.

Conclusions:

  • PPAR-γ agonists, particularly 15d-PGJ(2), demonstrate therapeutic efficacy in eosinophil-induced diseases.
  • These agonists exert their effects through modulation of Th2 patterns and alternative pathways involving IL-23/IL-17 and IL-33.
  • The findings suggest a novel mechanism for controlling eosinophil recruitment and associated pathologies.

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