Published ahead of print on January 18, 2005, doi:10.1164/rccm.200408-997OC
Am. J. Respir. Crit. Care Med., Volume 171, Number 8, April 2005, 829-837
A more recent version of this article appeared on April 15, 2005
Submitted on August 3, 2004
Accepted on January 12, 2005
Lung Parenchyma Remodeling in a Murine Model of Chronic Allergic Inflammation
Debora G Xisto1, Luciana L Farias2, Halina C Ferreira2, Miguel R Picanco2, Daniel Amitrano3, Jose R Lapa e Silva3, Elnara M Negri4, Thais Mauad5, Denise Carnielli5, Luiz Fernando F Silva4, Vera L Capelozzi5, Debora S Faffe2, Walter A Zin2, and Patricia RM Rocco1*
1 Carlos Chagas Filho Biophysics Institute, Laboratory of Pulmonary Investigation, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil,
2 Carlos Chagas Filho Biophysics Institute, Laboratory of Respiration Physiology, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil,
3 Clementino Fraga Filho University Hospital, Institute of Thoracic Diseases, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil,
4 Laboratory of Cellular Biology (LIM59), University of Sao Paulo, Sao Paulo, Brazil,
5 Department of Pathology, University of Sao Paulo, Sao Paulo, Brazil
* To whom correspondence should be addressed. E-mail: prmrocco{at}biof.ufrj.br.
This study tested the hypotheses that chronic allergic inflammation induces not only bronchial but also lung parenchyma remodeling, and that these histological changes are associated with concurrent changes in respiratory mechanics. For this purpose, airway and lung parenchyma remodeling were evaluated by quantitative analysis of collagen and elastin, immunohistochemistry (smooth-muscle actin expression, eosinophil, and dendritic cell densities), and electron microscopy. In vivo (airway resistance, viscoelastic pressure, and static elastance) and in vitro (tissue elastance, resistance, and hysteresivity) respiratory mechanics were also analyzed. BALB/c mice were sensitized with ovalbumin and exposed to repeated ovalbumin challenges. A marked eosinophilic infiltration was seen in lung parenchyma, large and distal airways. Neutrophils, lymphocytes, and dendritic cells also infiltrated the lungs. There was subepithelial fibrosis, myocyte hypertrophy and hyperplasia, elastic fiber fragmentation, and increased number of myofibroblasts in airways and lung parenchyma. Collagen fiber content was increased in the alveolar walls. The volume proportion of smooth-muscle-specific actin was augmented in distal airways and alveolar duct walls. Airway resistance, viscoelastic pressure, static elastance, tissue elastance and resistance were significantly increased. In conclusion, prolonged allergen exposure induced remodeling not only of the airway wall, but also of the lung parenchyma, leading to in vivo and in vitro mechanical changes.
Key words: Tissue mechanics, collagen, remodeling, actin
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