Effects of ozone exposure on nuclear factor-kappa B activation and tumor necrosis factor-alpha expression in human nasal epithelial cells

In this study we investigated a possible mechanism of the human airway infl ammatory response to inhaled ozone (O-3). Cultures of human nasal epithelia l (HNE) cells, initiated from excised nasal turbinates and grown on collage n-coated Transwell (R) tissue culture inserts, were exposed to 120, 240, or 500 ppb O-3 for 3 h. An electron spin resonance (ESR) signal that changed with time suggested free radical production in HNE cells exposed to O-3. Nu clear protein extracts were analyzed for the activated transcription factor NF-kappaB by electrophoretic mobility-shift assay (EMSA), and showed a sma ll dose-response activation of NF-kappaB that coincided with O-3-induced fr ee radical production. Basal media were analyzed for the presence of tumor necrosis factor-alpha (TNF-alpha) using the enzyme-linked immunosorbent ass ay (ELISA). In cultures exposed to 120 ppb O-3, the mean TNF-a concentratio n was not significantly different from those exposed to air. However, expos ure to 240 and 500 ppb O-3 significantly increased mean TNF-alpha expressio n, relative to controls, 16 h after exposure. These results support the hyp othesis that the human airway epithelium plays a role in directing the infl ammatory response to inhaled O-3 via free radical-mediated NF-kappaB activa tion.