Erratum: 15-Deoxy-Δ^12,14-Prostaglandin J₂ Induces IL-8 and GM-CSF in a Human Airway Epithelial Cell Line (NCI-H₂₉₂)

Background: 15-Deoxy-Δ^12,14-prostaglandin J₂ (15d-PGJ₂), a major prostanoid metabolized from prostaglandin D₂ (PGD₂), plays an important role in various biological processes including inflammatory responses. 15d-PGJ₂ exerts its effects through two major receptors, chemoattractant receptor- homologous molecule expressed on Th2 cells (CRTH2) and peroxisome proliferator-activated receptor-γ (PPARγ). The 15d-PGJ₂/PPARγ system, in particular, regulates numerous biological processes including adipogenesis, apoptosis, and inflammation. Although our studies have shown that PGD₂ (metabolic precursor of 15d-PGJ₂) induces IL-8 and GM-CSF production, the role of 15d-PGJ₂ (metabolite of PGD₂) is unknown in human bronchial epithelial cells. In this study, we investigated the function of 15d-PGJ₂ on a human airway epithelial cell line: NCI-H₂₉₂. Method: NCI-H₂₉₂ cells were cultured in the presence of various stimulants. The resulting supernatants were used for ELISA analysis. Results: We demonstrated that 15d-PGJ₂ induced production of IL-8 and GM-CSF from NCI-H₂₉₂. 13,14-Dihydro-15-keto-PGD₂ (DK-PGD₂) (CRTH2 agonist) and troglitazone (PPARγ agonist) failed to increase the production of these cytokines. Pretreatment with ramatroban (CRTH2 antagonist) and GW9662 (PPARγ antagonist) did not reduce the production of these cytokines. 15d-PGJ₂ activated the ERK1/2 signaling pathway in a time-dependent manner. Conclusion: These data showed that 15d-PGJ₂ is a potent inducer of IL-8 and GM-CSF production through ERK1/2 kinase activation, but this is independent of CRTH2 or PPARγ activation.