Elsevier

Human Pathology

Volume 26, Issue 1, January 1995, Pages 53-61
Human Pathology

Original contribution
Significance of early intra-alveolar fibrotic lesions and integrin expression in lung biopsy specimens from patients with idiopathic pulmonary fibrosis

https://doi.org/10.1016/0046-8177(95)90114-0Get rights and content

Abstract

To study the pulmonary structural remodeling in idiopathic pulmonary fibrosis (IPF), ultrastructural, immunohistochemical, and light microscopic morphometric observations were made on 11 pulmonary biopsy specimens from patients with IPF. The morphometric study was done using sequentially cut tissue sections stained for keratin-alcian blue periodic acid-Schiff (PAS), fibronectin, and type IV collagen-alcian blue PAS. Most of the early fibrotic lesions, which were alcian blue-and fibronectin-positive, were intra-alveolar in location. Intra-alveolar fibrosis is considered to be essential for the fusion of alveolar walls in IPF. A strong reaction for integrin α5β1 and vinculin was found in epithelial cells and mesenchymal cells in areas of intra-alveolar fibrosis. These findings show that these cells are active in adhesion to fibronectin in areas of early intra-alveolar fibrosis. Some of the epithelial cells, including cytoplasmic hyaline-laden cells, showed evidence of inadequate adhesion to the extracellular matrix, and this may constitute one of the mechanisms of progression of fibrosis in IPF.

References (28)

  • J Roman et al.

    Fibronectin

  • J Roman et al.

    Expression of fibronectin, the integrin α5, and α-smooth muscle actin in heart and lung development

    Am J Respir Cell Mol Biol

    (1992)
  • WT Chen et al.

    Coupled expression and colocalization of 140K cell adhesion molecules, fibronectin, and laminin during morphogenesis and cytodifferentiation of chick lung cells

    J Cell Biol

    (1986)
  • SM Albelda

    Endothelial and epithelial cell adhesion molecules

    Am J Respir Cell Mol Biol

    (1991)
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