Expression of PPARgamma in eosinophils and its functional role in survival and chemotaxis

Immunol Lett. 2003 Apr 3;86(2):183-9. doi: 10.1016/s0165-2478(03)00003-8.

Abstract

Eosinophils play a pivotal role in the mechanism of allergic diseases including asthma. Interleukin-5 (IL-5) and eotaxin are critical cytokines/chemokines for eosinophil activation. Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that regulates lipid metabolism. Recent evidence has suggested that PPARgamma serves as a negative regulator in the immune system. In the present study, we investigated the expression of PPARgamma and effect of PPARgamma agonist on human eosinophils. We demonstrated that purified eosinophils and Eol-1 cells express PPARgamma at the mRNA and protein levels. The PPARgamma agonist troglitazone reduced the IL-5-stimulated, but not spontaneous, eosinophil survival in a concentration-dependent manner. Moreover, the eotaxin-directed eosinophil chemotaxis was dose-dependently inhibited by troglitazone. Our results suggest that the administration of the PPARgamma agonists thiazolidinediones could be a new therapeutic modality for the treatment of allergic diseases such as asthma.

MeSH terms

  • Apoptosis
  • Cell Line, Tumor
  • Chemokine CCL11
  • Chemokines, CC / pharmacology
  • Chemotaxis, Leukocyte* / drug effects
  • Chromans / pharmacology
  • Eosinophils / drug effects
  • Eosinophils / immunology*
  • Humans
  • Interleukin-5 / pharmacology
  • RNA, Messenger / metabolism
  • Receptors, Cytoplasmic and Nuclear / agonists
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Thiazolidinediones / pharmacology
  • Transcription Factors / agonists
  • Transcription Factors / metabolism*
  • Transcription Factors / physiology*
  • Troglitazone

Substances

  • CCL11 protein, human
  • Chemokine CCL11
  • Chemokines, CC
  • Chromans
  • Interleukin-5
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Thiazolidinediones
  • Transcription Factors
  • Troglitazone