Lung injury, inflammation, and inflammatory stimuli in rats exposed to ozone.
Lung injury, inflammation, and inflammatory stimuli in rats exposed to ozone.
复制标题
暴露于臭氧的大鼠的肺损伤、炎症和炎症刺激。
DOI：
10.1080/009841000156899
复制
发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Gupta,SK
中科院分区：
文献类型：
--
作者：
Bhalla,DK;Gupta,SK
The effects of ozone (O3) on airway epithelia, inflammation, and expression of inflammatory stimuli were investigated to delineate the mechanisms of inflam matory reactions relevant to lung injury. Because the airway responses to O3develop gradually, this investigation included a time-sequence analysis. Rats exposed for 3 h to 1 ppm O3were studied at 4-h intervals up to 20 h postexposure. Bronchoalveolar lavage fluid (BAL) was analyzed for albumin as an indicator of increased permeability, polymorphonuclear leukocytes (PMNs) to assess the inflammatory status, macrophage inflammatory protein-2 (MIP-2, an inflammatory chemokine), and cell adhesion molecules for their role in inflammation and PMN functions. The time-related increase in album in was matched by a similar significant increase for PMNs, MIP-2, and intercellular adhesion molecule-1 (ICAM-1). However, no marked change occurred for b-2 integrin (CD-18) and leukotriene B4(LTB4). The results establish a temporal correlation of epithelial permeability with changes in inflammatory activity and stimuli responsible for PMN recruitment in the lung. The observations of elevated MIP-2 and ICAM-1 levels are consistent with their role in injury and inflammation. An early expression of MIP-2 mRNA in BAL cells, that is, immediately post O3exposure, and the peak increase in BAL MIP-2 levels 4 h later support the chem otactic role of MIP-2 in PMN recruitm ent at 4- and 12-h time points. The rapid drop in MIP-2 and ICAM-1 levels appears to signal the termination of inflammatory cell recruitment, which is accompanied by an onset of recovery.
