Royce F H, Plopper C G
Department of Pediatrics, School of Medicine, University of California, Davis, Sacramento 95817, USA.
Exp Lung Res. 1997 Jan-Feb;23(1):51-64. doi: 10.3109/01902149709046047.
Short-term exposure to the air pollutant ozone results in severe injury to the nares, trachea, and centriacinus. Long-term exposure however, leads to a state of tolerance that is characterized by remodeling in the centriacinar airways and markedly reduced cell necrosis and inflammation. This remodeling consists of hypertrophy and hyperplasia of Clara cells with a 2- to 5-fold increase in the intracellular content of the major protein synthesized by the Clara cell, Clara cell secretory protein (CCSP). Previous in vitro studies suggest that CCSP may moderate inflammation and bind reactive cytotoxicants. This study tested whether acute and chronic exposure to ozone alters the normal level of expression of the CCSP gene. Rats were exposed to ozone, 1 ppm 8 h nightly, for up to 90 days. Immunohistochemistry demonstrated repopulation of the alveolar ducts with CCSP positive Clara cells and an increase in the intensity of immunoreactive CCSP within Clara cells. The results showed that (1) CCSP mRNA expression, GAPDH, and beta-actin do not change as a result of ozone injury, (2) mRNA levels are more variable as a result of ozone injury and (3) CCSP mRNA expression increases with age.
短期暴露于空气污染物臭氧会导致鼻腔、气管和终末细支气管严重损伤。然而，长期暴露会导致一种耐受状态，其特征是终末细支气管气道重塑，细胞坏死和炎症明显减轻。这种重塑包括克拉拉细胞肥大和增生，克拉拉细胞合成的主要蛋白质克拉拉细胞分泌蛋白（CCSP）的细胞内含量增加2至5倍。先前的体外研究表明，CCSP可能减轻炎症并结合反应性细胞毒素。本研究测试了急性和慢性暴露于臭氧是否会改变CCSP基因的正常表达水平。将大鼠暴露于臭氧中，每晚1 ppm，持续8小时，最长可达90天。免疫组织化学显示，肺泡导管中CCSP阳性克拉拉细胞重新分布，克拉拉细胞内免疫反应性CCSP强度增加。结果表明：（1）CCSP mRNA表达、甘油醛-3-磷酸脱氢酶（GAPDH）和β-肌动蛋白不会因臭氧损伤而改变；（2）由于臭氧损伤，mRNA水平变化更大；（3）CCSP mRNA表达随年龄增加。
