[Study on the rat airway epithelial cell injury induced by bacterial infection and its pathogenesis]

To explore the rat airway, especially small airway epithelium injury induced by Klebsiella pneumoniae infection and its pathogenesis.

A rat airway inflammation and COPD model was induced by repeated intranasal infection with Klebsiella pneumoniae. The injury changes were dynamically observed under SEM, TEM and LM. Actin, TNF-alpha, Fos, Jun protein and their mRNA expression levels in small airway epithelium were analyzed by immunohistochemistry and in situ hybridization. The changes of lung TNF-alpha content were examined by radioimmunoassay.

1 week after Klebsiella pneumoniae infection the epithelial cilia cohered, fell down, partially fell off and the tight intercellular connection destroyed. 2 and 4 weeks after the infection, the injury of bronchus epithelia worsened with pronounced chronic inflammation in all bronchi. The bronchioles walls became thickened, lumen narrowed and emphysema was noted. Compared with control group, TNF-alpha mRNA expression was higher (P < 0.01) in the 2nd and 4th week while TNF-alpha protein was higher at 4 weeks (P < 0.01). From 1st week after the infection, Fos protein and mRNA expression began to elevate (P < 0.01). TNF-alpha content of lung began to increase (P < 0.01) and kept at a higher level until the 8th week.

Repeated intranasal injection of a certain amount of Klebsiella pneumoniae can induce airway inflammation and emphysema. The main features of early airway epithelia injury are damage of cilia and intercellular junctions, the cause of which may be associated with changes in microfilament arrangement of epithelia. High expression of TNF-alpha protein in the airway epithelia and lung parallels with epithelium injury. Fos and Jun proteins may also play important roles in up-regulating the TNF-alpha protein.