递增浓度肿瘤坏死因子攻击下肺泡上皮细胞分泌IL-8水平变化

Release of interleukin-8 from alveolar epithelial cells induced by different concentration tumor necrosis factor-alpha in vitro

目的观察不同浓度肿瘤坏死因子攻击下肺泡上皮细胞（A549细胞）存活率和分泌IL-8水平变化。方法A549细胞分为对照组和实验组，分别采用不同浓度TNF-α攻击，培养24h后测定各组细胞存活率、上清IL-8水平。结果不同浓度TNF-α攻击均能明显抑制A549细胞生长，其中5000u·ml^-1浓度组细胞存活率降为（90．1±1．1）％。TNF-α攻击浓度由100u·ml^-1升至1000u·ml^-1时，A549细胞分泌IL-8量由9．1±3．5pg·ml^-1升至203．7±12．4pg·ml^-1，TNF-α攻击浓度超过5000u·ml^-1后IL-8分泌量开始下降。结论以100u·ml^-1～1000u·ml^-1之间浓度的TNF-α进行攻击，A549细胞IL-8分泌量与TNF-α浓度存在剂量一效应关系，反映了急性肺损伤／急性呼吸窘迫综合征状态下肺泡上皮细胞分泌炎性介质情况。

Objective To investigate the effect of tumor necrosis factor-alpha on the secretion of interleukin-8（IL-8） from alveolar epithelial cells（AS49） in vitro. Methods A549 cells were divided into five groups： one control group and four TNF-α groups. After 24 hours＇ culture,the livability of A549 cells and the secretion of IL-8 were measured by ELISA. Resuits The livability of TNF-αgroups were lower than that of the control group （5000 u· ml^- 1-TNF-α group） （90.1 ± 1. 1） % vs control group （97.9 ± 0.9） %. TNF-α induced a rapidly growing of interleukin-8 in the TNF-α group （ 1000u· ml^ - 1-TNF-α group 203.7 ± 12.4 pg· ml^- 1 vs control group 9.1 ± 3.5 pg· ml^- 1 ）. Conclusion When the concentration of TNF-α was 100 u· ml^-1- 1000 u· ml^-1, there was a dose-dependent fashion between the secretion IL-8 and the concentration of TNF-α, which reflects the state of alveolar type Ⅱ epithelial cell in acute luing injury/acute respiratory disease syndrome.