Ciglitazone inhibits cigarette smoke solution-induced inflammatory responses in human middle ear epithelial cells

• Published in: International journal of pediatric otorhinolaryngology 2012-08, Vol.76 (8), p.1136-1139
• Main Authors: Jun, Hyung Jin, Lim, Hyun Woo, Choi, June, Jung, Hak Hyun, Chae, Sung Won
• Format: Article
• Language: English
• Subjects: Blotting, Western; Cells, Cultured; COX-2; Cytokines - metabolism; Ear, Middle - drug effects; Ear, Middle - metabolism; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Human middle ear epithelial cells; Humans; Inflammation - chemically induced; Inflammation - drug therapy; Inflammation - physiopathology; Otitis media; Otitis Media - drug therapy; Otolaryngology; Pediatrics; Peroxisome proliferator activated receptor gamma; PPAR gamma - agonists; Real-Time Polymerase Chain Reaction; Smoking; Smoking - adverse effects; Thiazolidinediones - pharmacology; Thiazolidinediones - therapeutic use; TNF-α
• ISSN: 0165-5876; 1872-8464
• DOI: 10.1016/j.ijporl.2012.04.017

Abstract Objective Peroxisome proliferator activated receptor-γ (PPAR-γ), a member of the nuclear hormone receptor superfamily, plays an important role in the regulation of mucosal inflammation. The aim of this study was to investigate the anti-inflammatory effect of a PPAR-γ agonist, ciglitazone, on cigarette smoke solution (CSS)-induced inflammation in human middle ear epithelial cell lines (HMEECs). Design HMEECs with or without ciglitazone pre-treatment were exposed to CSS in order to induce the inflammatory response. The suppressive effect of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2(COX-2), were evaluated using real-time polymerase chain reaction and Western blotting. Results Stimulation with CSS at 40 μg/ml for 6 h resulted in a 4.1-fold increase in the expression of TNF-α mRNA in the HMEECs. CSS-induced up-regulation of TNF-α mRNA was decreased by more than 2.8-fold in cells pre-treated with ciglitazone. The up-regulation of COX-2 mRNA and increased COX-2 protein expression induced by CSS were also inhibited by more than 3.7-fold with ciglitazone pre-treatment. Conclusions These findings suggest that the inflammatory response induced by CSS could be inhibited by ciglitazone, a PPAR-γ agonist, in HMEECs. As such, PPAR-γ agonists may have therapeutic potential for the treatment of otitis media.