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OZONE-INDUCED RELEASE OF CYTOKINES AND FIBRONECTIN BY ALVEOLAR MACROPHAGES AND AIRWAY EPITHELIAL CELLS
Citation:
Devlin, R., H. Koren, M. Madden, T. Noah, AND K. McKinnon. OZONE-INDUCED RELEASE OF CYTOKINES AND FIBRONECTIN BY ALVEOLAR MACROPHAGES AND AIRWAY EPITHELIAL CELLS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-95/022.
Description:
Although airway epithelial cells appear damaged following exposure of humans and animals to ozone, the contribution of these cells to inflammation observed after ozone exposure is unclear. ince human airway cells are infrequently available for in vitro studies, we have investigated the possibility of using the BEAS human cell line derived from normal human bronchial epithelial cells as a model to study the interaction between ozone and airway epithelial cells. EAS cells can be grown and maintained on rigid, collagen-impregnated filter supports, and the interaction of cells with ozone facilitated by exposing them to the gas with medium below the support but no medium on top of the cells. xposure of BEAS cells to concentrations of ozone ranging from 0.1 - 1.0 ppm resulted in the vectorial release of several inflammatory mediators, wit@ some of the mediators secreted apically and others primarily secreted basolaterally. here were significant increases in the amount of PGE2, PGF2 alpha, thromboxane, TC4, fibronectin, and IL-6 released following exposure of cells to zone. hus ozone stimulated the BEAS human bronchial epithelial cells to release many of the same inflammatory mediators that are detected in the bronchoalveolar lavage fluid of humans exposed to ozone, suggesting this cell line may be a useful tool to study human airway inflammation.