Association between Genetic Variants of Transforming Growth Factor-β1 and Susceptibility of Pneumoconiosis

Deng, Chonghai; Zhang, Xingxing; Lin, Jin‐Huan; Huang, Lifei; Qu, Yulan; Bai, Chong

doi:10.4103/0366-6999.198917

Cited by 9 publications

(8 citation statements)

References 37 publications

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“…The expression levels of the three related genes in the experimental groups increased, but their peak values appeared in different stages. In this study, the fact that the peak expression of collagen type I and III occurred after the peak expression of TGF-β1 indicated a possible causal relationship between these proteins: the total level of TGF-β1 secreted by BALF cells and lung tissues activated the expression of collagen type I and III, which was supported by the finding of previous studies 22 , 28 . This study also showed a different pattern of expression for collagen type I and III.…”

Section: Discussionsupporting

confidence: 88%

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO2-induced pulmonary fibrosis in rats in vivo

et al. 2019

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Silicosis is a serious occupational disease characterized by pulmonary fibrosis, and its mechanism and progression have not been fully elucidated yet. In this study, silicosis models of rat were established by a one-time dusting method, and the rats were sacrificed after 30, 60, and 120 days (herein referred to as the 30, 60, and 120 days groups, respectively). The rats without dust exposure were used as the control. The lungs were removed to observe pathological changes using hematoxylin and eosin and Masson’s trichrome staining and transmission electron microscopy, and the degree of collagen type I and III deposition in the lung was evaluated by enzyme‐linked immunosorbent assay. The levels of malondialdehyde and superoxide dismutase were measured by spectrophotometry, and the expression levels of fibrosis-related genes (transforming growth factor beta 1, type I collagen, type III collagen) were assessed by real-time quantitative polymerase chain reaction. The results suggested that the rats in the model groups exhibited obvious collagen fibrosis and that the severity of the lung injury increased as the time after exposure to SiO2 increased. There was a significant response to lung inflammation in the model rats, especially in the 30 days group. The degree of lipid peroxidation in bronchoalveolar lavage fluid cells and lung tissues in experiment group rats significantly increased. Among the three fibrosis-related genes, transforming growth factor beta 1was elevated in both bronchoalveolar lavage fluid cells and lung tissues of the experiment group rats, while collagen type I and III were only elevated in lung tissues. Hence, we concluded that as silicosis progressed, inflammation, fibrosis, and the expression of fibrosis-related genes showed different time-dependent changes and that a number of causal relationships existed among them.

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Section: Discussionsupporting

confidence: 88%

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO2-induced pulmonary fibrosis in rats in vivo

et al. 2019

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“…Previous research has described increased levels of inflammatory serum markers in silica exposed subjects 8 , 15 . It has been observed that the presence of different polymorphisms, alongside with TNF, IL-1RA and TGF-β1 16 – 18 confer a higher risk of disease, and that levels of TNF-α show an increase before the development of a clinically recognised silicosis 19 and that are associated with disease severity. Likewise, diverse studies associate TGF-β1 levels with disease progression and show that IL-2R can be a good indicator of silicosis-associated immunological alteration.…”

Section: Discussionmentioning

confidence: 99%

Serum levels of inflammatory mediators as prognostic biomarker in silica exposed workers

Blanco-Pérez

Blanco‐Dorado

Rodrı́guez-Garcı́a

et al. 2021

Sci Rep

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Silicosis is a diffuse interstitial lung disease caused by sustained inhalation of silica and silicates. Several cytokines are activated by their inhalation and can mediate the process of pulmonary fibrosis. The identification of biomarkers could allow an early diagnosis before the development of radiological alterations and help monitor the evolution of patients. The objetive of this study was to determine the clinical significance of specific biomarkers, to estimate their association with the development, severity and/or progression of silicosis, and identify determinants of this evolution. We conducted a prospective observational study in patients attending the pulmonology clinic from 2009 to 2018. Serum levels of the following inflammatory mediators were assessed: interleukin-6 (IL-6), interleukin 2 receptor subunit alpha (IL2R) interleukin 1 beta (IL1B), interleukin-8 (IL-8), tumour necrosis factor-alpha (TNF-α), transforming growth factor-beta1 (TGF-β1), alpha-1 antitrypsin (AAT), C-reactive protein (CRP), lactate dehydrogenase (LDH) and ferritin in subjects exposed to silica, with and without silicosis. Association between those inflammatory mediators with lung function measurements and radiological severity of disease and their impact on prognosis were analysed. 337 exposed to silica (278 with silicosis) and 30 subjects in the control group were included. IL-8, α1AT, ferritin, CRP and LDH levels were higher in silicosis than in those exposed to silica without silicosis. IL-8, LDH and AAT levels were associated with progression of silicosis and IL-6, IL-8, LDH, AAT, ferritin, and CRP with vital status. The results of the ROC analysis indicated the potential of IL-8 as a biomarker in the presence of silicosis and for the prediction of mortality.

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“…Current studies suggest that inflammatory processes play a key role in pneumoconiosis, which in turn promotes fibrosis progression. [ 68 , 69 ] The targets identified by omics are primarily focused on inflammatory signaling pathways relating to the immune system. When dust settles in the lungs, it activates an immune response.…”

Section: Future Research Prospectsmentioning

confidence: 99%

Pneumoconiosis: current status and future prospects

Luo

Song

et al. 2021

Chinese Medical Journal

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Pneumoconiosis refers to a spectrum of pulmonary diseases caused by inhalation of mineral dust, usually as the result of certain occupations. The main pathological features include chronic pulmonary inflammation and progressive pulmonary fibrosis, which can eventually lead to death caused by respiratory and/or heart failure. Pneumoconiosis is widespread globally, seriously threatening global public health. Its high incidence and mortality lie in improper occupational protection, and in the lack of early diagnostic methods and effective treatments. This article reviews the epidemiology, safeguard procedures, diagnosis, and treatment of pneumoconiosis, and summarizes recent research advances and future research prospects.

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Association between Genetic Variants of Transforming Growth Factor-β1 and Susceptibility of Pneumoconiosis

Cited by 9 publications

References 37 publications

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO<sub>2</sub>-induced pulmonary fibrosis in rats <i>in vivo</i>

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO<sub>2</sub>-induced pulmonary fibrosis in rats <i>in vivo</i>

Serum levels of inflammatory mediators as prognostic biomarker in silica exposed workers

Pneumoconiosis: current status and future prospects

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