Artigo Produção Nacional Revisado por pares

Lung Parenchyma Remodeling in a Murine Model of Chronic Allergic Inflammation

2005; American Thoracic Society; Volume: 171; Issue: 8 Linguagem: Inglês

10.1164/rccm.200408-997oc

ISSN

1535-4970

Autores

Débora G. Xisto, Luciana Landa Farias, Halina Cidrini Ferreira, Miguel Rossi Picanço, Daniel Amitrano, José Roberto Lapa e Silva, Eva Negri, Thaís Mauad, D. Carnielli, Luiz Fernando Ferraz da Silva, Vera Luíza Capelozzi, Débora S. Faffe, Walter A. Zin, Patrícia R. M. Rocco,

Tópico(s)

Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Resumo

This study tested the hypotheses that chronic allergic inflammation induces not only bronchial but also lung parenchyma remodeling, and that these histologic 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 and in 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 numbers 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, and 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.

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