using-nicotine-silica-exposed-mouse-model-to-promote-lung-epithelial

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Smoking and exposure to silica are common among occupational workers, and silica is more likely to injure the lungs of smokers than non-smokers. The role ...

a-silicosis-mouse-model-established-repeated-inhalation-crystalline

A Silicosis Mouse Model Established by Repeated Inhalation of Crystalline Silica Dust

Silicosis can be caused by exposure to respiratory crystalline silica dust (CSD) in an industrial environment. The pathophysiology, screening, and ...

Anhui University of Science and Technology

Anhui Province Engineering Laboratory of Occupational Health and Safety

To inquiry the effects of cigarette smoke extract(CSE) on RAW264. 7 cell proliferation, autophagy and its mechanism.

[Effect of cigarette smoke extract on RAW264. 7 cell proliferation, autophagy and its mechanism].

Coal dust particles (CDP), an inevitable by-product of coal mining for the environment, mainly causes coal workers' pneumoconiosis (CWP). Long-term exposure to coal dust leads to a complex alternation of biological processes during regeneration and repair in the healing lung. However, the cellular and complete molecular changes associated with pulmonary homeostasis caused by respiratory coal dust particles remain unclear.

Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies.

Pneumoconiosis patients exhibit significantly more anxiety and depression than healthy individuals. However, the mechanism of coal dust-induced anxiety and depression remains unclear.

Vitamin D3 suppresses astrocyte activation and ameliorates coal dust-induced mood disorders in mice.

As an infectious disease closely related to , autoimmunity, inflammation, environment and heredity, the relationship between the single nucleotide polymorphism of elongase 2 gene and the susceptibility to tuberculosis is still unknown.

Polymorphisms of Fatty Acid Elongase 2 Gene Afftects Risk of Pulmonary Tuberculosis in China Han Population.

Silicosis is an occupational disease that seriously damages the life and health of miners. Herein, we constructed a mouse model of silicosis and used label-free confocal Raman spectroscopy to analyze the biomolecular variations in lung fibrous nodules and inflammatory sites. The mice were exposed to silica particles for 1 month (SIL-1M group), 3 months (SIL-3M group), or no exposure (control tissues, NS). Raman spectra obtained from treated and untreated lung tissue were subjected to chemometric analysis to quantify biochemical composition differences in the silicosis. Simultaneously, immunohistochemistry and collagen staining were used to evaluate inflammation, fibrosis, and apoptosis. As a result, the SIL-1M and SIL-3M groups showed significant differences in cholesterol, lipids, amino acids, nucleic acids, and cytochrome C, and the collagen peaks at 1248 cm and 1448 cm were significantly higher than in the NS group. Notably, glycogen and phospholipid may be an inflammatory indicator consistent with NF-κB expression. In addition, significant differences in collagen and cytochrome C content in silicosis lung tissue were found using Raman spectroscopy and were verified by Masson's staining and Bax/Bcl-2 expression ratio. In summary, our findings provide a label-free technique to understand the biochemical changes in lung inflammatory and fibrosis microenvironment after exposure to silica particles and provide a valuable reference for studying the mechanism of silicosis.

Label-free Raman spectroscopy characterizes signatures of inflammation and fibrosis in the silicosis.

Coal workers' pneumoconiosis (CWP) is an occupational disease that severely damages the life and health of miners. However, little is known about the molecular and cellular mechanisms changes associated with lung inflammation and fibrosis induced by coal dust. As a non-destructive technique for measuring biological tissue, confocal Raman spectroscopy provides accurate molecular fingerprints of label-free tissues and cells. Here, the progression of lung inflammation and fibrosis in a murine model of CWP was evaluated using confocal Raman spectroscopy.

Inflammation and fibrosis in the coal dust-exposed lung described by confocal Raman spectroscopy.

Long-term coal dust exposure triggers complex inflammatory processes in the coal workers' pneumoconiosis (CWP) lungs. The progress of the inflammation is reported to be affected by disordered cell metabolism. However, the changes in the metabolic reprogramming associated with the pulmonary inflammation induced by the coal dust particles are unknown. Herein, we show that coal dust exposure causes glycogen accumulation and the reprogramming of glucose metabolism in the CWP lung. The glycogen accumulation caused by coal dust is mainly due to macrophages, which reprogram glycogen metabolism and trigger an inflammatory response. In addition, 2-deoxy-D-glucose (2-DG) reduced glycogen content in macrophages, which was accompanied by mitigated inflammation and restrained NF-κB activation. Accordingly, we have pinpointed a novel and crucial metabolic pathway that is an essential regulator of the inflammatory phenotype of coal dust-exposed macrophages. These results shed light on new ways to regulate CWP inflammation.

Glycogen metabolism reprogramming promotes inflammation in coal dust-exposed lung.

Silicosis is a severe pulmonary disease caused by inhaling dust containing crystalline silica. The progression of silicosis to pulmonary fibrosis is usually unavoidable. Recent studies have revealed positivity for the overexpression of C-X-C chemokine receptor type 4 (CXCR4) in pulmonary fibrosis and shown that the CXCR4 inhibitor AMD3100 attenuated pulmonary fibrosis after bleomycin challenge and paraquat exposure. However, it is unclear whether AMD3100 reduces crystalline silica-induced pulmonary fibrosis.

Article Total : 2	Year
Publication title	2023
Publication title	2023

Article	Year
[Effect of cigarette smoke extract on RAW264. 7 cell proliferation, autophagy and its mechanism]. Wei sheng yan jiu = Journal of hygiene research\| PubMed ID: 31875824	2019
Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies. Particle and fibre toxicology\| PubMed ID: 35057792	2022
Vitamin D3 suppresses astrocyte activation and ameliorates coal dust-induced mood disorders in mice. Journal of affective disorders\| PubMed ID: 35157949	2022
Polymorphisms of Fatty Acid Elongase 2 Gene Afftects Risk of Pulmonary Tuberculosis in China Han Population. Iranian journal of public health\| PubMed ID: 35223600	2021
Label-free Raman spectroscopy characterizes signatures of inflammation and fibrosis in the silicosis. Biochemical and biophysical research communications\| PubMed ID: 35344708	2022
Inflammation and fibrosis in the coal dust-exposed lung described by confocal Raman spectroscopy. PeerJ\| PubMed ID: 35765591	2022
Glycogen metabolism reprogramming promotes inflammation in coal dust-exposed lung. Ecotoxicology and environmental safety\| PubMed ID: 35907323	2022
C-X-C-Chemokine-Receptor-Type-4 Inhibitor AMD3100 Attenuates Pulmonary Inflammation and Fibrosis in Silicotic Mice. Journal of inflammation research\| PubMed ID: 36238768	2022

Yuanjie Zou

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