Eosinophils play a pivotal role in the mechanism of allergic diseases. The peroxisome proliferator-activated receptors (PPARs) are a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors. To date, three mammalian subtypes have been identified, referred to as PPAR⍺, β, and γ, which are encoded by separate genes. Among them, PPARγ is expressed at high levels in adipocytes and regulates adipose differentiation. Hematopoietic cells such as human monocytes, macrophages, and lymphocytes also express PPARγ. Most of the function of PPARγ in these cells, including survival, chemotaxis, cytokine production, and etc., are inhibitory. The expression and function of PPARγ in eosinophils are unclear so far.

Blood eosinophils were purified using Percoll and anti-CD16 antibody-coated magnetic beads. Expression of PPARγ was examined by RT-PCR and Western blotting. Eosinophil survival was analyzed by Annexin V and PI stainings. Chemotaxis assay was performed using Boyden chamber. CD69 expression of eosinophils was analyzed by flow cytometry. EDN release was measured by ELISA.

Eosinophils expressed PPARγ at the mRNA and protein levels. To elucidate the role of PPARγ in eosinophil function, we used the pharmacological agonists of PPARγ thiazolidinedions (troglitazone and pioglitazone). Both agonists significantly inhibited the eosinophil survival and chemotaxis in a dose-dependent manner. The IL-5-induced CD69 expression and EDN release were also reduced by the agonists.

Our results suggest that PPARγ negatively regulates eosinophil function. The pharmacological targeting of PPARγ can be a new strategy to treat allergic diseases such as asthma.