Abstract
Studies investigating association between tumor necrosis factor (TNF) gene polymorphisms and silicosis susceptibility report conflicting results. The aim of this meta-analysis was to assess association between TNF gene polymorphisms and silicosis susceptibility. A systematic literature search was conducted to find relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of association. Finally, a total of 12 articles, involving 1990 silicosis patients and 1898 healthy controls were included in the meta-analysis. Overall, meta-analysis revealed a significant association between the TNF −308A allele and silicosis (OR = 1.348, 95%CI = 1.156–1.570, P<0.001). A significant association of AA+AG genotype of the TNF −308 A/G polymorphism with susceptibility to silicosis was also found (OR = 1.466, 95%CI = 1.226–1.753, P<0.001). After stratification by ethnicity, significant associations were detected under the genetic models (A allele and AA+AG genotype) for TNF −308A/G polymorphisms in the Asian population (P<0.05). Similarly, meta-analysis of the TNF −238A/G polymorphism revealed the same pattern as that shown by meta-analysis of TNF −308A/G. The meta-analysis suggests that the TNF −308A/G and −238A/G polymorphisms are associated with susceptibility to silicosis, especially in Asians.
Highlights
Silicosis is an interstitial lung disease prevalent among miners, sand blasters, and quarry workers, manifested as a chronic inflammatory response leading to severe pulmonary fibrotic changes [1]
Silicosis is pneumoconiosis of lung fibrosis caused by inhalation of silica particles usually at low levels but for long periods
It is a common occupational disease among the workers who are exposed to silica particles
Summary
Silicosis is an interstitial lung disease prevalent among miners, sand blasters, and quarry workers, manifested as a chronic inflammatory response leading to severe pulmonary fibrotic changes [1] It is characterized by fibrotic nodules, thickening of the alveolar interstitium, and accumulation of inflammatory cells in the lung. Cytokines and fibrogenic mediators were released into the local tissues and triggered an inflammatory response, followed by fibroblast proliferation and collagenization [7] In this regard, tumor necrosis factor (TNF)-α derived from alveolar macrophages in the lung is important in regulating these mediators in silicosis. TNF-α is an important pro-inflammatory cytokine, secreted primarily by mononuclear phagocytic cells [8] It is involved in various physiologic and pathologic processes, such as inflammation initiation, immuno-regulation, proliferation, and apoptosis [9].
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