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Cytokine polymorphisms in silicosis and other pneumoconioses.

Authors
Yucesoy-B; Vallyathan-V; Landsittel-DP; Simeonova-P; Luster-MI
Source
Mol Cell Biochem 2002 May-Jun; 234-235(1-2):219-224
NIOSHTIC No.
20022965
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-alpha) 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.
Keywords
Silicosis; Pneumoconiosis; Coal-workers; Coal-workers-pneumoconiosis; Lung-disease; Lung-disorders; Growth-factors; Silica-dusts; Silicates; Dust-particles; Dusts; Particulate-dust; Particulates; Respiratory-system-disorders; Pulmonary-system-disorders
Contact
M.I. Luster, Toxicology and Molecular Biology Branch, NIOSH, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
MCBIB8
CAS No.
7631-86-9
Publication Date
20020501
Document Type
Journal Article
Email Address
mluster@cdc.gov
Fiscal Year
2002
NTIS Accession No.
NTIS Price
Issue of Publication
1-2
ISSN
0300-8177
NIOSH Division
HELD
Priority Area
Disease and Injury; Asthma and Chronic Obstructive Pulmonary Disease
Source Name
Molecular and Cellular Biochemistry
State
WV
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