RNA Therapeutics, Roche, Nutley, NJ 07110, USA.
Inflammation. 2010 Jun;33(3):144-56. doi: 10.1007/s10753-009-9168-5.
We investigated the cellular and molecular effects of ozone exposure in Cynomolgus monkeys. Thirty-six Cynomolgus monkeys were exposed to single or repeat ozone challenge. Pulmonary inflammation was assessed using bronchoalveolar lavage fluid (BAL) and histology. Gene expression profiling in lung and blood was performed. Ozone challenge evoked BAL cellular inflammation and increases in total protein, alkaline phosphatase and cytokines. Lung histology revealed cellular inflammation and epithelial necrosis. Gene expression profiling identified oxidative phosphorylation, immune response and cell adhesion pathways altered in response to ozone, with common and unique profiles in lung and blood. Lipocalin 2, CD177, the FK-506 and S100A8 binding proteins and ST-2 represent novel peripheral biomarkers of ozone toxicity. Repeat ozone challenge evoked reproducible inflammation but attenuated cell damage. These studies provide data on the molecular mechanisms and biomarker identification of ozone-evoked toxicity, and support the use of the Cynomolgus monkey as a model of human ozone challenge.
我们研究了臭氧暴露对食蟹猴的细胞和分子影响。36 只食蟹猴接受了单次或重复的臭氧挑战。通过支气管肺泡灌洗(BAL)和组织学评估肺部炎症。对肺和血液中的基因表达谱进行了分析。臭氧挑战引起 BAL 细胞炎症和总蛋白、碱性磷酸酶和细胞因子增加。肺组织学显示细胞炎症和上皮坏死。基因表达谱分析表明,臭氧反应改变了氧化磷酸化、免疫反应和细胞黏附途径,在肺和血液中有共同和独特的特征。脂联素 2、CD177、FK-506 和 S100A8 结合蛋白以及 ST-2 是臭氧毒性的新型外周生物标志物。重复臭氧挑战引起可重复的炎症,但减轻了细胞损伤。这些研究提供了臭氧诱发毒性的分子机制和生物标志物识别的数据,并支持使用食蟹猴作为人类臭氧挑战的模型。