[In vitro exposure of a human bronchial epithelial cell line with nitrogen dioxide induces enhanced transcription and liberation of pro-inflammatory cytokines].

Studies of in vivo inhalation of nitrogen dioxide (NO2) have demonstrated a transient pulmonary inflammation. This study was done to determine the contribution of airway epithelial cells to the release of inflammatory mediators following NO2 exposure. Confluent cultures of the human bronchial epithelial cell line BEAS-2B on Transwell-Col filters were exposed for 1 h to air or NO2 up to 1.5 ppm with the apical fluids removed with 5% CO2 at 37 degrees C. The cells were hydrated with Hanks' Balanced Salt Solution (HBSS) in the basolateral compartment. Sequential reverse transcription and quantitative cDNA amplification (RT-PCR) was used to measure inflammatory mediator mRNA abundance in BEAS-2B cultures. When compared to air-exposed cells, NO2 induced increases in IL-6 (23.4-fold) and IL-8 (30.9-fold) mRNA abundance. The NO2-dependent increases in mRNA expression reached a maximum between 0 and 1 h post exposure and returned to baseline levels within 24 h. IL-6 and IL-8 proteins as measured by enzyme-linked immunosorbent assays (ELISA) were also elevated in supernatants recovered from NO2-exposed BEAS-2B cells. These studies suggest that exposure to NO2 induces the synthesis and release of inflammatory mediators from airway epithelial cells that may participate in the pathogenesis of airway disease.