Mycoplasma pneumoniae infection increases airway collagen deposition in a murine model of allergic airway inflammation

Chu, Hong Wei, John G. Rino, Rachel B. Wexler, Krista Campbell, Ronald J. Harbeck, and Richard J. Martin. Mycoplasma pneumoniae infection increases airway collagen deposition in a murine model of allergic airway inflammation. Am J Physiol Lung Cell Mol Physiol 289: L125-L133, 2005. First published March 18, 2005; doi:10.1152/ajplung.00167.2004.-Mycoplasma pneumoniae (Mp) has been linked to chronic asthma. Airway remodeling (e. g., airway collagen deposition or fibrosis) is one of the pathological features of chronic asthma. However, the effects of respiratory Mp infection on airway fibrosis in asthma remain unclear. In the present study, we hypothesized that respiratory Mp infection may increase the airway collagen deposition in a murine model of allergic airway inflammation in part through upregulation of transforming growth factor (TGF)-beta 1. Double (2 wk apart) inoculations of Mp or saline (control) were given to mice with or without previous allergen (ovalbumin) challenges. On days 14 and 42 after the last Mp or saline, lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analyses of collagen and TGF-beta 1 at protein and mRNA levels. In allergen-naive mice, Mp did not alter airway wall collagen. In allergen-challenged mice, Mp infections did not change airway wall collagen deposition on day 14 but increased the airway collagen on day 42; this increase was accompanied by increased TGF-beta 1 protein in the airway wall and reduced TGF-beta 1 protein release from the lung tissue into BAL fluid. Our results suggest that Mp infections could modulate airway collagen deposition in a murine model of allergic airway inflammation with TGF-beta 1 involved in the collagen deposition process.