Interleukin-18, interleukin-8, and CXCR2 and the risk of silicosis

Abstract

Molecular mechanisms in the pathogenesis of silicosis are not fully understood. Exposure to crystalline silica leads to the activation of signaling pathways controlling the production and secretion of inflammatory mediators. Inflammatory cytokines are noted as important candidate genes for fibrotic lung diseases. Cytokines, chemokines, and variations of their genes have been associated with upregulation or downregulation of chronic inflammatory mediators. Variations in the interleukin (IL)-18, IL-8 and chemokine receptor CXCR2 genes are believed to influence the risk of silicosis in stone-grinding factory workers in Iran. Allele-specific oligonucleotide polymerase chain reaction (PCR) procedure was carried out for IL-18 −137 and IL-18 −607, meanwhile touchdown PCR was performed for IL-8 −251 and CXCR2 +1208 genotyping. Variation in genotypic and allelic frequencies was not statistically different among cases versus controls ( p > 0.05). These findings indicated for the first time that IL-18 −137, IL-18 −607, IL-8 −251, and CXCR2 +1208 are suggested not to influence the risk of silicosis in tested occupational group.