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Cytokine polymorphisms in silicosis and other pneumoconiosis

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Oxygen/Nitrogen Radicals: Cell Injury and Disease

Part of the book series: Developments in Molecular and Cellular Biochemistry ((DMCB,volume 37))

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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)

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Yucesoy, B., vallyathan, V., Landsittel, D.P., Simeonova, P., Luster, M.I. (2002). Cytokine polymorphisms in silicosis and other pneumoconiosis. In: Vallyathan, V., Shi, X., Castranova, V. (eds) Oxygen/Nitrogen Radicals: Cell Injury and Disease. Developments in Molecular and Cellular Biochemistry, vol 37. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1087-1_25

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  • DOI: https://doi.org/10.1007/978-1-4615-1087-1_25

  • Publisher Name: Springer, Boston, MA

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