Cytokine polymorphisms in silicosis and other pneumoconioses.
Yucesoy-B; Vallyathan-V; Landsittel-DP; Simeonova-P; Luster-MI
Mol Cell Biochem 2002 May-Jun; 234-235(1-2):219-224
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.
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
M.I. Luster, Toxicology and Molecular Biology Branch, NIOSH, 1095 Willowdale Road, Morgantown, WV 26505, USA
Disease and Injury; Asthma and Chronic Obstructive Pulmonary Disease
Molecular and Cellular Biochemistry