The Synthetic PPARγ Agonist Troglitazone Inhibits IL-5-Induced CD69 Upregulation and Eosinophil-Derived Neurotoxin Release from Eosinophils

Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear receptor that regulates lipid metabolism. Recently, PPARγ was reported to be a negative regulator in the immune system. Eosinophils also express PPARγ, however, the role of PPARγ in eosinophil functions is not well understood. Surface expression of CD69 and eosinophil-derived neurotoxin (EDN) release are well-known activation markers of eosinophils. We investigated the effect of a PPARγ agonist on human eosinophil functions such as IL-5-induced CD69 surface expression and EDN release. IL-5 significantly induced eosinophil CD69 surface expression analyzed using flow cytometry and EDN release measured by ELISA. IL-5-induced eosinophil CD69 surface expression and EDN release were significantly inhibited by the synthetic PPARγ agonist troglitazone, and these effects were reversed by a PPARγ antagonist. The PPARγ agonist troglitazone has a potent inhibitory effect on activation and degranulation of eosinophils, and it may be a therapeutic modality for the treatment of allergic diseases.