FUNCTION OF IL8 AND NEUTROPHILS AFTER OZONE INJURY

臭氧是光化学烟雾的主要成分，也是全球最重要的空气污染物之一。 短期臭氧暴露会导致肺上皮坏死，主要是腺泡中心区域的I型细胞和纤毛细胞。 最近的实验研究表明，嗜酸性细胞流入，其进展到上皮损伤部位，有助于去除坏死的上皮细胞并加速上皮修复。 IL-8的产生被臭氧暴露的气道上皮细胞上调，但其相对于中性粒细胞流入的功能尚未明确。 中性粒细胞运输到臭氧损伤区域并帮助清除臭氧损伤的气道上皮细胞的机制尚不清楚。 永生化和原代人和恒河猴支气管上皮细胞体外臭氧暴露后，将研究以下具体目标：1）表征在暴露于环境水平的臭氧后产生IL-8的气道上皮细胞的表型2）确定中性粒细胞是否直接迁移到臭氧损伤的气道上皮细胞3）确定IL-8是否在呼吸道上皮细胞中表达。暴露于环境水平臭氧的气道上皮细胞产生的β 8与嗜中性粒细胞的共定位相关。

Ozone is a major component of photochemical smog and one of the most important air pollutants worldwide. Short-term ozone exposure causes epithelial necrosis in the lung, primarily of type I and ciliated cells in centriacinar regions. Recent experimental investigations have shown that the neutrophilic influx, which progresses to sites of epithelial injury, aids in the removal of necrotic epithelial cells and expedites epithelial repair. IL-8 production is upregulated by ozone exposed airway epithelium, but its' function relative to the neutrophil influx is not well defined. The mechanisms by which neutrophils traffic to an area of ozone injury and aid in the removal of ozone injured airway epithelial cells are unknown. After in vitro ozone exposure of immortalized and primary human and Rhesus monkey bronchial epithelial cells, the following specific aims will be investigated: 1) characterize the phenotype of the airway epithelial cell(s) that produce IL-8 after exposure to ambient levels of ozone 2) determine whether neutrophils migrate directly to ozone injured airway epithelial cells 3) determine if IL-8 production by airway epithelium exposed to ambient levels of ozone correlates with the co-localization of neutrophils.