To analyze the bronchial epithelial cell damage induced by Mycoplasma pneumonia and the therapeutic effects of clarithromycin, we observed bronchial tissue damage by using a mouse model and performing immunostaining a...To analyze the bronchial epithelial cell damage induced by Mycoplasma pneumonia and the therapeutic effects of clarithromycin, we observed bronchial tissue damage by using a mouse model and performing immunostaining and scanning electron microscopy. The immunostaining study showed that M. pneumoniae-labeled fluorescence was found on the mucosal epithelium of mice, 6 days after inoculation. Clarithromycin treatment reduced the fluorescence. In this study, we demonstrated that the morphological alterations of bronchial mucosa, including the shortening and loss of ciliavisualized by scanning electron microscopy, and the inflammatory cell migration in the submucosal tissue visualized by differential interference contrast microscopy, were induced by mycoplasmal infection. We also showed that clarithromycin treatment, when administered from the first day of inoculation, attenuated both the bronchial epithelial damage and inflammatory cell migration in the submucosal tissue. These results suggest that the therapeutic effects of clarithromycin against mycoplasmal infection, may be due to its antibacterial and anti-inflammatory activities.展开更多
文摘To analyze the bronchial epithelial cell damage induced by Mycoplasma pneumonia and the therapeutic effects of clarithromycin, we observed bronchial tissue damage by using a mouse model and performing immunostaining and scanning electron microscopy. The immunostaining study showed that M. pneumoniae-labeled fluorescence was found on the mucosal epithelium of mice, 6 days after inoculation. Clarithromycin treatment reduced the fluorescence. In this study, we demonstrated that the morphological alterations of bronchial mucosa, including the shortening and loss of ciliavisualized by scanning electron microscopy, and the inflammatory cell migration in the submucosal tissue visualized by differential interference contrast microscopy, were induced by mycoplasmal infection. We also showed that clarithromycin treatment, when administered from the first day of inoculation, attenuated both the bronchial epithelial damage and inflammatory cell migration in the submucosal tissue. These results suggest that the therapeutic effects of clarithromycin against mycoplasmal infection, may be due to its antibacterial and anti-inflammatory activities.
