Apoptosis and extracellular matrix remodelling in human silicosis

Histopathology. 2006 Sep;49(3):283-9. doi: 10.1111/j.1365-2559.2006.02477.x.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Collagen / metabolism
  • Elastic Tissue / metabolism
  • Extracellular Matrix / metabolism*
  • Fas Ligand Protein
  • Humans
  • Image Processing, Computer-Assisted
  • Immunohistochemistry
  • Mast Cells / cytology
  • Membrane Glycoproteins / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Silicosis / metabolism*
  • Silicosis / pathology*
  • Tumor Necrosis Factors / biosynthesis

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Necrosis Factors
  • Collagen