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Plasma Cytokine Profiling Reveals Differences Between Silicotic Patients with Simple Silicosis and Those with Progressive Massive Fibrosis Caused by Engineered Stone

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2023 Jan 21
PMID 36675056
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Abstract

Engineered stone silicosis has become an occupational epidemic disease that progresses rapidly to progressive massive fibrosis with respiratory failure and death, and there is no effective treatment. Silica deposition in the lung triggers a series of inflammatory reactions with the participation of multiple cytokines and cellular mediators whose role in the development and progression of the disease is largely unknown. We hypothesized that differences in plasma cytokine levels exist between patients diagnosed with simple silicosis (SS) and patients diagnosed with progressive massive fibrosis (PMF). Plasma samples from 91 ES silicosis patients, diagnosed and classified by chest radiography and/or high-resolution computed tomography with SS ( = 53) and PMF ( = 38), were assayed by multiplex assays for levels of 34 cytokines. Additionally, a healthy volunteer control group ( = 22) was included. Plasma levels of a high number of cytokines were significantly higher in subjects with silicosis than in healthy control subjects. Moreover, the levels of IL-1RA, IL-8, IL-10, IL-16, IL-18, TNF-α, MIP-1α, G-CSF and VEGF were significantly elevated in PMF compared to SS patients. This study shows that plasma cytokine levels differ between healthy people and silicosis patients, and some of them are also significantly elevated in patients with PMF compared with patients with SS, which could indicate their involvement in the severity of the disease, be considered as biomarkers and could be explored as future therapeutic targets for the disease.

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Unveiling the threat of crystalline silica on the cardiovascular system. A comprehensive review of the current knowledge.

Gurzu I, Handra C, Ghita I, Otelea M Front Cardiovasc Med. 2025; 12:1506846.

PMID: 40027509 PMC: 11868085. DOI: 10.3389/fcvm.2025.1506846.

References
1.
Nakanishi K . Unique Action of Interleukin-18 on T Cells and Other Immune Cells. Front Immunol. 2018; 9:763. PMC: 5920033. DOI: 10.3389/fimmu.2018.00763. View

2.
Song X, Shi Y, You J, Wang Z, Xie L, Zhang C . D-4F, an apolipoprotein A-I mimetic, suppresses IL-4 induced macrophage alternative activation and pro-fibrotic TGF-β1 expression. Pharm Biol. 2019; 57(1):470-476. PMC: 6691790. DOI: 10.1080/13880209.2019.1640747. View

3.
Chaudhary N, Roth G, Hilberg F, Muller-Quernheim J, Prasse A, Zissel G . Inhibition of PDGF, VEGF and FGF signalling attenuates fibrosis. Eur Respir J. 2007; 29(5):976-85. DOI: 10.1183/09031936.00152106. View

4.
Heinzerling A, Cummings K, Flattery J, Weinberg J, Materna B, Harrison R . Radiographic Screening Reveals High Burden of Silicosis among Workers at an Engineered Stone Countertop Fabrication Facility in California. Am J Respir Crit Care Med. 2020; 203(6):764-766. DOI: 10.1164/rccm.202008-3297LE. View

5.
Wu C, Luo Z, Pang B, Wang W, Deng M, Jin R . Associations of Pulmonary Fibrosis with Peripheral Blood Th1/Th2 Cell Imbalance and EBF3 Gene Methylation in Uygur Pigeon Breeder's Lung Patients. Cell Physiol Biochem. 2018; 47(3):1141-1151. DOI: 10.1159/000490208. View