ALTERATION OF ALVEOLAR MACROPHAGE CHEMOTAXIS, CELL-ADHESION, AND CELL-ADHESION MOLECULES FOLLOWING OZONE EXPOSURE OF RATS

Ozone (O-3) exposure of humans and animals induces an inflammatory res ponse in the lung, which is associated with macrophage stimulation, re lease of chemotactic agents, and recruitment of polymorphonuclear leuk ocytes (PMNs). This study was designed to investigate the functional a spects of the macrophages that impact inflammatory processes in the lu ng. Macrophages recovered by bronchoalveolar lavage (BAL) from rats ex posed to purified air or 0.8 ppm O-3 were studied for their chemotacti c activity, adhesive interactions with alveolar epithelial cells in cu lture, surface morphology, and surface expression of cell adhesion mol ecules. The macrophages isolated from O-3-exposed rats exhibited a gre ater motility in response to a chemotactic stimulus than the macrophag es isolated from rats exposed to purified air. The macrophages from O- 3-exposed animals also displayed greater adhesion when placed in cultu re with epithelial cells isolated from adult rat lung (ARL-14) than th e macrophages from control rats. Both chemotactic motility and cell ad hesion stimulated by O-3 exposure were attenuated when the macrophages were incubated in the presence of monoclonal antibodies to leukocyte adhesion molecules, CD11b, or epithelial cell adhesion molecules, ICAM -1. Flow cytometry revealed a modest increase in the surface expressio n of CD11b but no change in ICAM-1 expression in macrophages from O-3- exposed rats when compared to those from the air-exposed controls. The results demonstrate an alteration of macrophage functions following O -3 exposure and suggest the dependence of these functions on the biolo gic characteristics, rather than the absolute expression, of the cell adhesion molecules. (C) 1996 Wiley-Liss, Inc.