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Peroxisome proliferator-activated receptor-gamma is deficient in alveolar macrophages from patients with alveolar

Tracey L Bonfield1, Carol F Farver, Barbara P Barna

  • 1Department of Pulmonary and Critical Care Medicine, 9500 Euclid Avenue, Cleveland Clinic Foundation, Desk A90, Cleveland, OH 44195-5038. thomasm@ccf.org

American Journal of Respiratory Cell and Molecular Biology
|June 14, 2003
PubMed

Insights

Granulocyte macrophage colony-stimulating factor (GM-CSF) therapy restores peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and CD36 levels in pulmonary alveolar proteinosis (PAP) patients. This suggests GM-CSF regulates lung homeostasis through PPAR-gamma-dependent pathways, offering new insights into PAP treatment.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a nuclear transcription factor regulating lipid and glucose metabolism and inflammation.
  • Granulocyte macrophage colony-stimulating factor (GM-CSF) is crucial for lung homeostasis, potentially influencing surfactant clearance.
  • The role and activation status of PPAR-gamma in human alveolar macrophages, particularly in pulmonary alveolar proteinosis (PAP), remain undefined.

Purpose of the Study:

  • To investigate the expression and regulation of PPAR-gamma and its target gene CD36 in alveolar macrophages from healthy individuals and PAP patients.
  • To determine the effect of GM-CSF on PPAR-gamma and CD36 expression in PAP.
  • To elucidate the potential role of GM-CSF-regulated PPAR-gamma pathways in maintaining lung homeostasis.

Main Methods:

  • Quantitative analysis of PPAR-gamma mRNA and protein expression in alveolar macrophages from healthy controls and PAP patients.
  • Assessment of CD36 expression in alveolar macrophages.
  • In vivo studies involving GM-CSF therapy in PAP patients to evaluate its impact on PPAR-gamma and CD36 levels.

Main Results:

  • PPAR-gamma and CD36 were found to be highly expressed in alveolar macrophages of healthy subjects but severely deficient in PAP patients.
  • The deficiency of PPAR-gamma and CD36 in PAP alveolar macrophages was not intrinsic and could be restored by GM-CSF therapy.
  • GM-CSF treatment in PAP patients normalized PPAR-gamma levels to those observed in healthy controls.

Conclusions:

  • GM-CSF plays a critical role in regulating PPAR-gamma expression in alveolar macrophages.
  • GM-CSF therapy effectively restores PPAR-gamma and CD36 levels in PAP, suggesting a therapeutic potential.
  • A novel hypothesis is proposed: GM-CSF regulates lung homeostasis via PPAR-gamma-dependent pathways.

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