Alveolar epithelial cells secrete chemokines in response to IL-1β and lipopolysaccharide but not to ozone
Alveolar epithelial cells secrete chemokines in response to IL-1β and lipopolysaccharide but not to ozone
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DOI：
10.1165/rcmb.2005-0205oc
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发表时间：
2006-02-01
影响因子：
6.4
通讯作者：
Mason, RJ
中科院分区：
文献类型：
--
作者：
Manzer, R;Wang, JR;Mason, RJ
臭氧暴露产生急性炎症和远端肺中性粒细胞内流。肺泡上皮细胞覆盖很大的表面积，分泌趋化因子，并可能引发或改变炎症反应。臭氧对这些细胞产生趋化因子的影响尚未确定。在不同条件下培养离体大鼠II型细胞，表达I型和II型细胞表型的形态外观和生化标志物。这些细胞暴露在空气/液体界面的臭氧中。i型细胞比II型细胞更容易受到损伤，并且在100ppb臭氧暴露60分钟时表现出损伤迹象。通过测量8-异前列腺素的产生，两种表型在臭氧暴露后都显示了脂质过氧化的证据，但两种表型都没有分泌增加的MIP-2 (CXCL3), cnc -1 （CXCL1）或MCP-1 （CCL2）。两种细胞表型均分泌MIP-2和MCP-1以响应IL-1 β或脂多糖，但与臭氧没有启动或协同作用。肺泡间室对臭氧的炎症反应很可能不是由于臭氧对上皮细胞的直接作用。
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-1 beta 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.