Manzer Rizwan, Wang Jieru, Nishina Kahoru, McConville Glen, Mason Robert J
Department of Medicine, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.
Am J Respir Cell Mol Biol. 2006 Feb;34(2):158-66. doi: 10.1165/rcmb.2005-0205OC. Epub 2005 Oct 20.
Ozone exposure produces acute inflammation and neutrophil influx in the distal lung. Alveolar epithelial cells cover a large surface area, secrete chemokines, and may initiate or modify the inflammatory response. The effect of ozone on chemokine production by these cells has not been defined. Isolated rat type II cells were cultured in different conditions to express the morphologic appearance and biochemical markers for the type I and the type II cell phenotypes. These cells were exposed to ozone at an air/liquid interface. The type I-like cells were more susceptible to injury than the type II cells and showed signs of injury at exposure levels of 100 ppb ozone for 60 min. Both phenotypes showed evidence of lipid peroxidation after ozone exposure as measured by 8-isoprostane production, but neither phenotype secreted increased amounts of MIP-2 (CXCL3), CINC-1 (CXCL1), or MCP-1 (CCL2) in response to ozone. Both cell phenotypes secreted MIP-2 and MCP-1 in response to IL-1beta or lipopolysaccharide, but there was no priming or synergy with ozone. It is likely that the inflammatory response to ozone in the alveolar compartment is not due to the direct effect of ozone on epithelial cells.
臭氧暴露会在肺远端产生急性炎症和中性粒细胞流入。肺泡上皮细胞覆盖大面积，分泌趋化因子，并可能启动或改变炎症反应。臭氧对这些细胞趋化因子产生的影响尚未明确。分离的大鼠II型细胞在不同条件下培养，以表达I型和II型细胞表型的形态学外观和生化标志物。这些细胞在气液界面暴露于臭氧。I型样细胞比II型细胞更容易受到损伤，在100 ppb臭氧暴露60分钟时就出现损伤迹象。通过8-异前列腺素生成测定，两种表型在臭氧暴露后均显示脂质过氧化证据，但两种表型对臭氧均未分泌增加量的MIP-2（CXCL3）、CINC-1（CXCL1）或MCP-1（CCL2）。两种细胞表型对IL-1β或脂多糖均分泌MIP-2和MCP-1，但与臭氧无启动或协同作用。肺泡腔对臭氧的炎症反应可能不是由于臭氧对上皮细胞的直接作用。
