Decreased Soluble Receptor of Advanced Glycation End Product Levels Correlated with Inflammation in Silicosis

Liu, Heliang; Ma, Jie; Tian, Jiang; Li, Enhong; Zhao, Xiaokun; Wang, Ying; Cui, Jie; Hao, Xiaohui; Guo, Lingli

doi:10.1155/2020/2683753

Cited by 5 publications

(7 citation statements)

References 50 publications

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“…Alveolar macrophage is the primary immune cell that recognizes and engulfs silica particles (Leung et al, 2012;Mossman and Churg, 1998). Macrophages activated by silica particles demonstrate enhanced pro-inflammatory cytokine production, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α) and IL-6, which play central roles in the inflammatory response and the accumulation of lung collagen (Piguet et al, 1990;Tripathi et al, 2010;Liu et al, 2020). In animal models, suppressing pro-inflammatory cytokine pro-duction effectively inhibited silica-induced inflammation, even the fibrotic responses (Di Giuseppe et al, 2009;Guo et al, 2013;Sato et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Exogenous Clara cell protein 16 attenuates silica particles-induced inflammation in THP-1 macrophages by down-regulating NF-κB and caspase-1 activation

Cui

Zhang

et al. 2020

J. Toxicol. Sci.

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Inhalation of silica particles leads to pulmonary inflammatory responses. Clara cell protein 16 (CC16) has been reported to played a protective role in inflammatory lung diseases. However, its role on silica particles-induced inflammation has not been fully clarified. In this study, THP-1 macrophages were exposed to 75 μg/cm 2 silica particles with or without 2 μg/mL exogenous CC16 (recombinant CC16, rCC16) for 24 hr. The production of inflammatory cytokines, including interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6, in the cell supernatants of different groups was detected through ELISA kits and real-time RT-PCR, respectively. The nuclear translocation of nuclear factor (NF)-κB, protein levels of pro-IL-1β, the nucleotide-binding domain-like receptor protein 3 (NLRP3) and caspase-1 were evaluated via immunofluorescence or western blot. Results showed that, at 75 μg/cm 2 silica particle concentration, the treatment of rCC16 significantly decreased IL-1β, TNF-α and IL-6 protein release and mRNA levels in THP-1 macrophages. Compared to those only exposed to silica particles, THP-1 macrophages exposed to both silica particles and rCC16 showed significantly lower nuclear levels and higher cytosol levels of NF-κB p65, as well as lower co-localization coefficients through immunofluorescence. Additionally, the administration of rCC16 significantly attenuated the increase of pro-IL-1β, NLRP3 and caspase-1 levels induced by silica particle exposure. Our results suggested that exogenous CC16 could inhibit silica particles-induced inflammation in THP-1 macrophages, mainly through suppressing NF-κB pathway and caspase-1 activation.

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Section: Introductionmentioning

confidence: 99%

Exogenous Clara cell protein 16 attenuates silica particles-induced inflammation in THP-1 macrophages by down-regulating NF-κB and caspase-1 activation

Cui

Zhang

et al. 2020

J. Toxicol. Sci.

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“…A meta-analysis for each of the three cytokines was performed. The publication dates for the studies used in the meta-analysis ranged from 1994 to 2021 (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). In total, the 11 studies combined were comprised of 547 control (healthy) participants and 938 patients with pneumoconiosis.…”

Section: Resultsmentioning

confidence: 99%

Elevated levels of IL-8, TGF-β, and TNF-α associated with pneumoconiosis: A meta-analysis

Chen,

Syed

2022

J Emerg Invest

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There have been multiple studies over the years looking into the role of cytokines, which are regulators of inflammation in the development of pneumoconiosis. The aim of this study to determine whether serum levels of certain cytokines can be useful as biomarkers for pneumoconiosis. To date, the most investigated cytokines have been Interleukin 8 (IL-8), transforming growth factor beta 1 (TGF-β1), and tumor necrosis factor alpha (TNF-α). Results from previous studies generally show that the serum levels of these cytokines are altered in pneumoconiosis, however not all of these deviations are statistically significant. Here we attempt to determine whether levels of IL-8, TGF-β1, and TNF-α are significantly related to pneumoconiosis, by conducting a meta-analysis of 11 studies on the serum levels of three cytokines: IL-8, TGF-β1, and TNF-α. The meta-analysis concluded that pneumoconiosis patients display significantly elevated levels of IL-8 and TNF-α. The meta-analysis for serum TGF-β1 in pneumoconiosis patients failed to reach statistical significance. The results of the meta-analysis suggest that serum levels of IL-8 and TNF-α could be utilized in the diagnosis of pneumoconiosis, and further studies should be conducted to investigate the correlation strength of these two cytokines with pneumoconiosis.

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“…Studies found that TNF-α and IL-6 were increased in the serum [ 27 ] and BALF [ 28 ] of patients with silicosis. TGF-β1 and CTGF, two classical pro-fibrotic cytokines, were also found to increase in serum of patients with silicosis and lung tissues of silicotic rat [ 29 – 31 ]. Similarly, our study found that the secretion of serum TGF-β1, CTGF, TNF-α and IL-6 were higher in patients with silicosis than in healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

The significance of serum S100 calcium-binding protein A4 in silicosis

Zhang

Yuan

et al. 2022

BMC Pulm Med

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Background Silicosis is a chronic occupational pulmonary disease characterized by persistent inflammation and irreversible fibrosis. Considerable evidences now indicate that S100 calcium-binding protein A4 (S100A4) has been associated with fibrotic diseases. However, the role of S100A4 in silicosis is still unclear. Methods In this study, serum levels of S100A4, transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) in patients with silicosis (n = 42) and control group (CG, n = 12) were measured by ELISA. S100A4 expression in lung tissues and primary alveolar macrophages (AMs) of mice with and without silicosis was detected by immunohistochemistry (IHC)/real-time PCR. The correlations between S100A4 and cytokines or lung function were assessed by Spearman's rank correlation analyses. Results Compared with CG, the levels of S100A4 were significantly increased in silicosis patients (70.84 (46.22, 102.46) ng/ml vs (49.84 (42.86, 60.02) ng/ml). The secretions of TGF-β1, CTGF, IL-6 and TNF-α in silicosis group were significantly higher than that in control group (p < 0.05). Serum S100A4 levels were positively correlated with TGF-β1 and IL-6, while were negatively correlated with lung function parameters including percentage of predicted forced vital capacity (FVC%pre), maximum vital capacity (Vcmax), deep inspiratory capacity (IC) and peak expiratory flow at 75% of vital capacity (PEF75). In receiver operating characteristic (ROC) analyses, S100A4 > 61.7 ng/ml had 63.4% sensitivity and 83.3% specificity for silicosis, and the area under the curve (AUC) was 0.707. Furthermore, immunostaining of lung tissues showed the accumulation of S100A4-positive cells in the areas of nodules of silicotic mice. The mRNA expression of S100A4 in the lung tissues and AMs of silicotic mice were significantly higher than controls. Conclusion These data suggested that increased S100A4 might contribute to the pathogenesis of silicosis.

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Decreased Soluble Receptor of Advanced Glycation End Product Levels Correlated with Inflammation in Silicosis

Cited by 5 publications

References 50 publications

Exogenous Clara cell protein 16 attenuates silica particles-induced inflammation in THP-1 macrophages by down-regulating NF-κB and caspase-1 activation

Exogenous Clara cell protein 16 attenuates silica particles-induced inflammation in THP-1 macrophages by down-regulating NF-κB and caspase-1 activation

Elevated levels of IL-8, TGF-β, and TNF-α associated with pneumoconiosis: A meta-analysis

The significance of serum S100 calcium-binding protein A4 in silicosis

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