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Apoptosis and extracellular matrix remodelling in human silicosis
Author(s) -
Delgado L,
Parra E R,
Capelozzi V L
Publication year - 2006
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2006.02477.x
Subject(s) - silicosis , extracellular matrix , inflammation , pathology , fas ligand , apoptosis , lung , mast cell , immunohistochemistry , fibrosis , extracellular , chemistry , medicine , immunology , biology , microbiology and biotechnology , programmed cell death , biochemistry
Aims: Silicosis is a chronic occupational disease caused by the inhalation of free crystalline silica particles which produce inflammation and tissue destruction followed by remodelling of the extracellular matrix. Apoptosis has been implicated in the development of the initial inflammation that triggers the remodelling process. Our aim was to elucidate the importance of Fas‐ligand (Fas‐L) in this disorder and to study the relationship between Fas‐L and several other inflammatory and fibrotic remodelling markers. Methods and results: We analysed 23 lung biopsies from silicotic patients and five controls, quantifying Fas‐L and Bcl‐2 expression by inflammatory cells as well as mast cells and collagen and elastic fibres. We used immunohistochemistry and morphometry to evaluate the amount of Fas‐L and Bcl‐2. Our analysis revealed that the silicotic lung stage was significantly related to Fas‐L, mast cell and extracellular matrix remodelling. Fas‐L expression was inversely associated with mast cells, collagen/elastic deposition and the silicotic lung. Conclusion: Fas‐L, mast cell staining and collagen/elastic fibre quantities in silicotic lungs are strongly related to silicosis progression.