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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/L125    most recent 00167.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Chu, H. W. Articles by Martin, R. J. Search for Related Content PubMed PubMed Citation Articles by Chu, H. W. Articles by Martin, R. J.

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

Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colorado

Submitted 10 May 2004 ; accepted in final form 11 March 2005

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)-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-1 at protein and mRNA levels. In allergen-naïve 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-1 protein in the airway wall and reduced TGF-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-1 involved in the collagen deposition process.

transforming growth factor-1

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