Yucesoy Berran, Vallyathan Val, Landsittel Douglas P, Simeonova Petia, Luster Michael I
Ankara University, Faculty of Pharmacy, Department of Toxicology, Turkey.
Mol Cell Biochem. 2002 May-Jun;234-235(1-2):219-24.
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.
矽肺和煤工尘肺是复杂的多因素肺部疾病，其发病机制尚未完全明确。一般认为，肺纤维化疾病是由巨噬细胞衍生的细胞因子和生长因子介导的。有证据表明肿瘤坏死因子-α（TNF-α）和白细胞介素-1（IL-1）在二氧化硅粉尘引起的炎症以及从单纯性到进行性大块纤维化的转变过程中起关键作用。在本综述中，我们讨论了负责调节这些促炎细胞因子产生的基因多态性及其在改变矽肺严重程度中的作用。
