Abstract
Silicosis is a devastating disease caused by inhalation of silica dust that leads to inflammatory cascade and then scarring of the lung tissue. Increasing evidences indicate that soluble receptor for advanced glycation end products (sRAGE) is involved in inflammatory diseases. However, no data on the possible relationship between sRAGE and inflammation of silicosis are available. In this study, serum from subjects with silicosis (n = 59) or from healthy controls (HC, n = 14) was analyzed for the secretion of sRAGE, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), and oxidized low-density lipoprotein (ox-LDL). The associations between sRAGE and cytokines and ox-LDL and lung function were assessed by Pearson's correlation analyses. Mean levels of serum sRAGE were lower in silicosis than those in controls (p < 0.05). The subjects who had a longer term of occupational exposure had higher levels of sRAGE (p < 0.05). The secretion of TNF-α, IL-1β, IL-6, TGF-β1, and ox-LDL was significantly higher in the silicosis group than that in the HC group (p < 0.05). Furthermore, the levels of sRAGE were negatively correlated with TNF-α, IL-6, IL-1β, and ox-LDL. There is no correlation between sRAGE and TGF-β1 and lung function. The optimal point of sRAGE for differentiating silicosis from healthy controls was 14250.02 pg/ml by ROC curve analysis. A decrease in serum sRAGE and its association with inflammatory response might suggest a role for sRAGE in the pathogenesis of silicosis.
Highlights
Silicosis is one of the most important occupational diseases worldwide [1], while no clinically available therapy is able to revert the progression of the disease effectively [2]
Since circulating Soluble receptor for advanced glycation end products (sRAGE) may be a biomarker during chronic inflammation, we tested sRAGE levels by ELISA in serum from patients with silicosis in this study
Using Receiver operating characteristic (ROC) analysis, we found that 14250.02 pg/ml was the best serum sRAGE cut-off level to distinguish between healthy controls and silicosis patients (AUC = 0:713) (Figure 4)
Summary
Silicosis is one of the most important occupational diseases worldwide [1], while no clinically available therapy is able to revert the progression of the disease effectively [2]. After silica is inhaled, alveolar macrophages (AMs) are activated to release inflammatory cytokines and fibrotic cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and transforming growth factor-β1 (TGF-β1) [7,8,9,10], which play crucial roles in inflammatory response and fibrosis of silicosis. Receptor for advanced glycation end products (RAGE), a pattern-recognition receptor, has been reported to amplify or sustain immune and inflammatory responses [15,16,17] and drive fibrotic process [18]. Studies have found that sRAGE have a protective effect against inflammation through inhibiting RAGE signaling [23, 24]. SRAGE has been recognized as a biomarker or therapeutic target in inflammatory diseases
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