摘要
目的观察重度烟雾吸入后大鼠急性肺损伤(ALI)早期肺泡巨噬细胞(AM)的活性、分泌功能,探讨其在ALI免疫调控中的意义。方法复制重度烟雾吸入致大鼠早期重度吸入性损伤模型。健康Wister大鼠36只,按随机数字表法分为对照组及创伤后2、4、6、12和24h组。免疫细胞化学方法(ICC)鉴定肺组织中巨噬细胞特异性表型CD68的表达,收集AM培养上清液,用酶联免疫吸附试验(ELISA)分别检测TNF-α、IL-6、IFN-γ和IL-10的浓度。结果在肺损伤的早期(2h)即出现肺泡巨噬细胞的激活且程度与时间呈正相关;AM分泌TNF-α的能力在早期(2h)即出现迅速上升,2h达高峰,6h后逐渐下降至正常。4hIL-6、IFN-γ开始出现持续高表达,6h时AM分泌IL-10的能力开始增强且后期(24h)出现异常增高。结论AM的激活是发生急性肺损伤的一个重要的起动信号,且持续时间及严重程度与肺损伤程度明显呈正相关;AM通过对其分泌的一些关键性的细胞因子的调节参与了对肺损伤中的免疫调控。
Objective To investigate the activation and secretion ability of alveolar macrophage and its regulatory role in immunoregulation following smoke inhalation-induced acute lung injury in rat.Methods Smoke inhalation-induced lung injury model should be replicated.Thirty-six healthy Wister rats were randomly divided into normal control group and 2、4、6、12 and 24 h groups after trauma.Alveolar macrophages were identified by immunocytochemistry.Different secretion abilities of TNF-α,IL-6,IL-10 and IFN-γ of AM were detected by enzyme linked immunosorbent assay（ELISA）.Results Alveolar macrophage activation increased at 2 h,duration and intensity were positively correlated to time.Secretion ability of TNF-α increased immediately after trauma and reached the peak value at 2 h and gradually drop to normal after 6 h＇s injury.Secretion ability of IL-6 and IFN-γ increased obviously at 4 h and keep a high level from the period of 4 h to 24,whereas the secretion ability of IL-10 increased at 6 h and increased abnormality at 24 h.Conclusion Activation of alveolar macrophage may be regarded as a key initiation signal for acute lung injury.Duration and intensity of activation of alveolar macrophage determine the severity acute lung injury.Through regulation the secretion ability of some key cytokines,alveolar macrophage actually participates in immunoregulation during acute lung injury.
出处
《安徽医科大学学报》
CAS
北大核心
2008年第5期500-503,共4页
Acta Universitatis Medicinalis Anhui
基金
全军"十五"攻关课题(编号:04M009)
