Ozone Can Increase the Expression of Intercellular Adhesion Molecule-1 and the Synthesis of Cytokines by Human Nasal Epithelial Cells

Publisher Website
Google Scholar
Abstract
Ozone is a highly toxic and ubiquitous air pollutant that induces epithelial cell injury and airway inflammation. This study examined the effects of sublethal, near ambient ozone concentrations on the expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and the synthesis of certain cytokines by human nasal epithelial cells (HNE). The cytokines studied were interleukin-lα (IL-1α), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNFα). The HNE were cultured and exposed to ozone in an environment that simulated that of the human airway. Cells were grown and exposed on microporous filters and were assayed for ICAM-1 expression in an adherent state with a laser cytometer. Dual-wavelength detection using a fltiorescein-conjugated antibody to detect receptor expression and propidium iodide to count cell nuclei allowed measurement of ICAM-1 expression on individual cells, expressed as fluorescence per cell. The IL-lα, IL-6, IL-8, and TNFα were measured in HNE culture supernatants by two-site enzyme-linked immunosorbant assays (ELISA). Exposure of the HNE to 0.50 ppm ozone for 6 h increased ICAM-1 expression by 36 ± 11%. In comparison, culturing these cells with interferon-gamma (IFNyγ increased ICAM-1 expression by 179 ± 52%. Exposure of HNE to ozone at the same concentration and duration increased the release of IL-1(α by 262 ± 44%, IL-6 by 72 ± 67%, and TNFα by 162 ± 120%. Following exposure to 0.50 ppm ozone there was no change in the release of IL-8; however, the constitutive synthesis of this cytokine was very high. No changes in either ICAM-1 expression or cytokine release were seen after exposure of HNE to 0.25 ppm ozone for 6 h. These results suggest that airway inflammation that is a consequence of ozone exposure may result at least in part from concomitant increases in epithelial ICAM-1 and cytokine expression and subsequent leukocyte—epithelial interactions.