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首页> 外文期刊>Journal of Cellular Physiology >Alteration of alveolar macrophage chemotaxis, cell adhesion, and cell adhesion molecules following ozone exposure of rats.
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Alteration of alveolar macrophage chemotaxis, cell adhesion, and cell adhesion molecules following ozone exposure of rats.

机译：变更肺泡巨噬细胞趋化作用的细胞粘附,细胞粘附分子老鼠的臭氧接触。

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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.
机译：臭氧(O3)接触引发的人类和动物肺部炎症反应,这是与巨噬细胞刺激,释放趋化因子和招聘的多形核白细胞(中性粒细胞)。旨在调查的功能方面的巨噬细胞的影响肺的炎症过程。恢复了支气管肺泡灌洗(BAL)大鼠暴露于净化空气或0.8 ppm O3为他们的趋化现象的研究活动,胶粘剂与肺泡上皮细胞的相互作用文化、表面形态和表面细胞粘附分子的表达。从O3-exposed老鼠巨噬细胞分离表现出更大的能动性在回答比巨噬细胞趋化现象的刺激分离大鼠暴露于净化空气。巨噬细胞从O3-exposed动物也显示更大的粘附在文化与上皮细胞分离成年大鼠肺(ARL-14)比控制的巨噬细胞老鼠。刺激O3曝光时衰减巨噬细胞是孵化的存在白细胞粘附的单克隆抗体上皮细胞粘附分子,CD11b或分子,ICAM-1。适度增加表面的表达CD11b ICAM-1表达但没有变化巨噬细胞从O3-exposed老鼠相比那些从air-exposed控制。表明巨噬细胞功能的改变后O3曝光和建议的依赖性这些功能的生物特征,而不是绝对的细胞粘附分子的表达。

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