Neutrophils enhance removal of ozone-injured alveolar epithelial cells in vitro.
Neutrophils enhance removal of ozone-injured alveolar epithelial cells in vitro.
复制标题
中性粒细胞在体外增强臭氧损伤的肺泡上皮细胞的清除。
作者：
J. M. Cheek;R. Mcdonald;L. Rapalyea;B. Tarkington;D. Hyde
在体内急性暴露于氧化性气体后，肺上皮中炎性细胞的迁移和积聚与上皮细胞坏死相一致。本研究的目的是定量测试的假设，即静止的中性粒细胞增强清除氧化剂损伤的肺上皮细胞暴露于臭氧在体外。原代分离的大鼠肺泡II型细胞培养为单层，使用无血清培养基。暴露于0.1-0.5 ppm臭氧0.5小时后，单层细胞的顶侧仅给予新鲜营养培养基或含有静止的人中性粒细胞的培养基。单层生物电特性和细胞摄取的活性染料记录从5至48小时后臭氧暴露。臭氧剂量依赖性的单层通透性增加与比例较高的损伤上皮细胞的数量。然而，臭氧暴露后的单层通透性的中性粒细胞的影响的方向和幅度依赖于臭氧浓度。此外，与仅暴露于低水平臭氧的单层细胞相比，暴露于0.1 ppm臭氧的嗜铬细胞瘤处理的单层细胞对活体染料摄取呈阳性的附着细胞显著减少;这种效应随着臭氧浓度的增加而减弱。这些数据表明，在高水平的臭氧中性粒细胞可能会加剧氧化损伤的上皮细胞的损伤，而暴露于环境浓度的臭氧后，中性粒细胞的存在可能会加快上皮屏障功能的恢复。我们的结论是，通过增强损伤细胞的清除，中性粒细胞可以促进修复后，臭氧暴露在体内的中央腺泡上皮。
After acute exposure to oxidant gases in vivo, migration and accumulation of inflammatory cells in pulmonary epithelium coincides with epithelial cell necrosis. The present study was designed to test quantitatively the hypothesis that quiescent neutrophils enhance the removal of oxidant-injured pulmonary epithelial cells after exposure to ozone in vitro. Primary isolated rat alveolar type II cells were cultured as monolayers, using serum-free medium. After exposure to 0.1-0.5 ppm ozone for 0.5 h, apical sides of monolayers were administered either fresh nutrient medium only or medium containing quiescent human neutrophils. Monolayer bioelectric properties and cellular uptake of vital dye were recorded from 5 to 48 h after ozone exposure. Ozone dose-dependent increases in monolayer permeability were associated with proportionally higher numbers of injured epithelial cells. However, the direction and magnitude of neutrophil effects on monolayer permeability after ozone exposure were dependent on ozone concentration. Furthermore, neutrophil-treated monolayers exposed to 0.1 ppm ozone had significantly fewer attached cells positive for uptake of vital dye relative to monolayers exposed to the low level of ozone only; this effect was ablated with increasing ozone concentration. These data suggest that at high levels of ozone neutrophils may exacerbate injury to oxidant-impaired epithelial cells, whereas the presence of neutrophils after exposure to ambient concentrations of ozone may expedite the restoration of epithelial barrier function. We conclude that, by enhancing the removal of injured cells, neutrophils may facilitate the repair of centriacinar epithelium after ozone exposure in vivo.