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Cytokine polymorphisms in silicosis and other pneumoconiosis

  • Berran Yucesoy
  • Val vallyathan
  • Douglas P. Landsittel
  • Petia Simeonova
  • Michael I. Luster
Chapter
  • 405 Downloads
Part of the Developments in Molecular and Cellular Biochemistry book series (DMCB, volume 37)

Abstract

Silicosis and coal workers’ pneumoconiosis are complex multifactorial lung diseases whose etiopathogenesis are not well defined. It is generally accepted that fibrotic lung disorders are mediated by macrophage-derived cytokines and growth factors. There is evidence showing a crucial role for tumor necrosis factor-a (TNF-a) and interleukin-1 (IL-1) in inflammation caused by silica dust and in the transition from simple to progressive massive fibrosis. In this review we discuss genetic polymorphisms responsible for regulating the production of these proinflammatory cytokines and their role in modifying silicosis severity. (Mol Cell Biochem 234/235: 219–224, 2002)

Key words

silicosis pneumoconiosis cytokines polymorphism TNF-a 

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Copyright information

© Springer Science+Business Media New York 2002

Authors and Affiliations

  • Berran Yucesoy
    • 1
  • Val vallyathan
    • 2
  • Douglas P. Landsittel
    • 3
  • Petia Simeonova
    • 4
  • Michael I. Luster
    • 4
  1. 1.Ankara UniversityFaculty of Pharmacy, Department of ToxicologyAnkaraTurkey
  2. 2.Pathology and Physiology Research BranchMorgantown
  3. 3.Biostatistics BranchMorgantown
  4. 4.Toxicology and Molecular Biology BranchHealth Effects and Laboratory Division, National Institute for Occupational Safety and HealthMorgantownUSA

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