Alteration of alveolar macrophage chemotaxis, cell adhesion, and cell adhesion molecules following ozone exposure of rats

Abstract

Ozone (O3) exposure of humans and animals induces an inflammatory response in the lung, which is associated with macrophage stimulation, release of chemotactic agents, and recruitment of polymorphonuclear leukocytes (PMNs). This study was designed to investigate the functional aspects of the macrophages that impact inflammatory processes in the lung. Macrophages recovered by bronchoalveolar lavage (BAL) from rats exposed to purified air or 0.8 ppm O3 were studied for their chemotactic activity, adhesive interactions with alveolar epithelial cells in culture, surface morphology, and surface expression of cell adhesion molecules. The macrophages isolated from O3-exposed rats exhibited a greater motility in response to a chemotactic stimulus than the macrophages isolated from rats exposed to purified air. The macrophages from O3-exposed animals also displayed greater adhesion when placed in culture with epithelial cells isolated from adult rat lung (ARL-14) than the macrophages from control rats. Both chemotactic motility and cell adhesion stimulated by O3 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 expression of CD11b but no change in ICAM-1 expression in macrophages from O3-exposed rats when compared to those from the air-exposed controls. The results demonstrate an alteration of macrophage functions following O3 exposure and suggest the dependence of these functions on the biologic characteristics, rather than the absolute expression, of the cell adhesion molecules.

In Vitro Multibiomarker Approaches for Assessing the Immunotoxicity of Certain Sections in Yangtze River

“…Studies have provided evidence for the assumption that altered properties on the cell surface of macrophages, e.g., changes in cell adhesion and surface extensions, are highly relevant to the inflammation initiation process. 31 Here, we evaluated the effect of surface water on the morphology and adhesion of macrophages for the first time. We are of the opinion that these two bioassays are of high sensitivity and appropriate for assessing the surface water quality, since both are closely related to inflammation initiation, and altered significantly when treated with even 10× water extracts.…”

“…Similar to the results of adherence, four water extracts promoted an irregular appearance in THP-1 mφs. Studies have provided evidence for the assumption that altered properties on the cell surface of macrophages, e.g., changes in cell adhesion and surface extensions, are highly relevant to the inflammation initiation process . Here, we evaluated the effect of surface water on the morphology and adhesion of macrophages for the first time.…”

Adhesion molecules of blood polymorphonuclear leukocytes and alveolar macrophages in rats: modulation by exposure to ozone

“…Under different exposure conditions (3 h and 0.8 p.p.m., Sprague Dawley rats), Bhalla 8 found a substantial increase in the adhesiveness of AM to epithelial cells from ozone-exposed rats, but only a modest but signi®cant increase in the expression of CD11b on AM. Bhalla's explanation that the adhesive interactions in the ozone-induced in¯ammatory process do not require an increased number of CD11b/CD18 on AM, but that the adhesive behavior might depend on factors other than a simple upregulation of cell adhesion molecules, does not contradict our results.…”

An Automated System for Exposure of Cultured Cells and Other Materials to Ozone

“…Ozone exposure has been linked not only to increases in airway responsiveness but also to DNA damage and death of lung cells. Cell culture models have been used to address several aspects of ozone toxicity, including the effects of ozone on alveolar macrophage adhesion (Bhalla, 1996;Bhalla et al, 1996), cytokine production by alveolar macrophages (Arsalane et al, 1995;Devlin et al, 1994;Ishii et al, 1997;Pearson & Bhalla, 1997) and airway epithelial cells (Devlin et al, 1994;Jaspers et al, 1997;Leikauf et al, 1995;Rusznak et al, 1996), and epithelial cell barrier function (Cheek et al, 1994;Devlin et al, 1994;Jaspers et al, 1997;Leikauf et al, 1995;Rusznak et al, 1996). The study of cell culture models to elaborate the mechanism of ozone toxicity should be conducted under conditions of humidity, temperature, and pH very similar to those existing in vivo.…”