肺炎克雷伯菌引起大鼠小气道上皮细胞损伤及与肺内α肿瘤坏死因子关系的探讨

目的探讨肺炎克雷伯菌引起大鼠小气道上皮细胞损伤及机制。方法将Wistar大鼠随机分为两组:对照组和感染组采用光镜动态观察小气道上皮细胞损伤改变。以免疫组化及原位分子杂交分析方法,检测小气道上皮细胞α肿瘤坏死因子(TNF-α)蛋白和TNF-αmRNA表达的变化。并用放射免疫分析法测定肺组织中TNF-α含量。结果显示感染组大鼠小气道上皮细胞病理改变明显。感染第2周起至第4周小气道壁各种炎症细胞增加,可见上皮细胞部分脱落坏死,损伤明显加重。感染组在2～4周TNF-αmRNA表达与对照组比较显著增强(P <0 .0 1)。在第4周TNF α蛋白明显增高(P <0 .0 1)。从第1周起肺组织中TNF-α含量增加并保持到第8周。结论肺炎克雷伯菌在体内可引起小气道上皮细胞损伤,肺内TNF-α水平升高与气道上皮细胞损伤程度平行。并且TNF-α蛋白和TNF-αmRNA表达上调在加重上皮细胞损伤中又具有重要作用

Study on rat small airway epithelium injury induced by Klebsiella pneumoniae and relation with TNF-α in the lung

PurposeTo study rat small airway epithelium injury induced by Klebsiella pneumoniae infection and its pathogenesis.MethodsWistar rats were randomly divided into two groups:Conrtol group(group C) and Klebsiella pneumoniae infection group (group K).Were observed dynamically group K rat small airway epithelium injury changes under TEM. Were analysed rat small airway epithelium cell TNF-α protein and rnRNA expression level changes by immunohistochemistry and hybridization in situ. Lung TNF-α changes were examined by radioimmunoassay.ResultsIt is shown that group K rats had obviously pathologic changes 2 weeks to 4 weeks after infection,varied inflammatory cells of small airway wall obviously increased and epithelium surface local microvillus fall off was seen,and injury became obviously severe.TNF-α mRNA expression was higher (P<0.01) at 2 and 4 weeks than that of control group rats.TNF-α protein was higher at 4 weeks(P<0.01).From 1 week TNF-α content of lung began to increase (P<0.01)and kept higher until 8th week.ConclusionKlebsiella pneumonia can induce airway epithelium injury in vivo.Epithelium injury is correlated with higher level of lung TNF-α and TNF-α mRNA,TNF-α protein higher expression may play an important role in the process of trachea epithelium injury becoming obviously severe.