Advances in Microbiology

Volume 4, Issue 11 (September 2014)

ISSN Print: 2165-3402   ISSN Online: 2165-3410

Google-based Impact Factor: 1.18  Citations  h5-index & Ranking

Clarithromycin Attenuates the Bronchial Epithelial Damage Induced by Mycoplasma pneumoniae Infection

HTML  Download Download as PDF (Size: 3065KB)  PP. 697-703  
DOI: 10.4236/aim.2014.411075    3,155 Downloads   4,359 Views  Citations

ABSTRACT

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.

Share and Cite:

Tanaka, H. , Sadakata, H. , Nagami, T. , Miyazaki, S. , Tomita, T. , Shirata, S. and Yamagishi, T. (2014) Clarithromycin Attenuates the Bronchial Epithelial Damage Induced by Mycoplasma pneumoniae Infection. Advances in Microbiology, 4, 697-703. doi: 10.4236/aim.2014.411075.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.