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

Silicosis as the serious occupational disease is highly necessary to construct a suitable mouse model for disclosing mechanism of occurrence and development in this disease. Here, the volume-effect relationship and volume-based survival curves in mice who inhaled silica suspension intranasally were analyzed. Notable, the optimal volume 80 μl repeated-inhalation by nose to silica suspension in the inbred mouse C57BL/6 J with the highest susceptibility to silicosis led to a great entrance into the lung and a high survival rate after instillation. After repeated-exposure to 20 mg/mL, 80 μl silica for 16 days and then fed without silica exposure until 31 days, weight of mice showed a trend of first decrease and then recover. Moreover, the degree of pulmonary inflammation and fibrosis in mice were analyzed by pathological and immunohistochemistry staining. Transforming growth factor-beta (TGF-β), smooth muscle alpha-actin (α-SMA) and collagen type-I (collagen I, Col-I) were significantly increased in the silica-exposed mouse lung at post-exposure day 16 compared with the controls. Sirius red stain and Micro-CT analysis showed that lung fibrosis formed at post-exposure day 31. This study highlights the critical importance of perfusion volume and repeated nasal drops in inducing inflammatory response and pulmonary fibrosis in silicosis.

A suitable silicosis mouse model was constructed by repeated inhalation of silica dust via nose.

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.

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.

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
A suitable silicosis mouse model was constructed by repeated inhalation of silica dust via nose. Toxicology letters\| PubMed ID: 34626813	2021
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
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
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

Hangbing Cao

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