| Long term inhalation of coal dust in the working environment is still an issue in coal mine occupational safety and health.Coal dust induces inflammation and fibrosis in the lung,leading to pneumoconiosis in coal workers.At present,the pathogenesis of pneumoconiosis has not been completely understood,and there is no effective treatment to reverse its progress.Vitamin D is a healthy nutritional supplement that has been reported to play a beneficial role in various lung diseases.Here,a cross-sectional study was performed to assess the risks for the occupational hazards in a coal mine in northern Shanxi province,and the correlation between vitamin D level and lung function was analyzed.Moreover,serum inflammation and fibrosis factors were tested in the occupational population exposed to coal dust.To verify the findings in the human population and understand the underlying mechanism of pneumoconiosis,single-cell sequencing analysis of the coal mine dust-exposed lung,the vitamin D treated lung,and the control ones was performed in a mouse model with pneumoconiosis.It is found that the main occupational hazard factor in northern Shanxi coal mine is coal dust based on the coal dust monitoring data and occupational health risk assessment.However,79.3%rates of vitamin D deficiency were found in coal-dust exposure groups.After adjustment for confounders,a negative correlation between serum 25(OH)D3 levels and lung function was still found.Then,the expression levels of IL-1β,TGF-β,TNF-α,and COL3A1 in serum were detected by Elisa,the sensitivity and specificity of TGF-β,IL-1β,and COL3A1 were higher,and the screening effect was also better.Therefore,TGF-β,IL-1β,and COL3A1 can be used as potential indicators for early screening of coal lung disease.HE,Masson,Sirius red staining,and immunohistochemical staining were performed on lung tissue sections of mice with coal pneumoconiosis at different stages(1,6,and 9 months).The results showed that inflammatory reaction and fibrosis increased in coal dust mice.However,the levels of α-SMA,F4/80,Fibronectin,1L-6 in the lung tissue of mice treated with vitamin D were lower than those in the coal dust group,otherwise,anti-inflammatory cytokine 1L-10 were higher than control group.Using single-cell sequencing,we found that 9-month coal dust stimulation induces an increase in HAAS,a group of highly active alveolar type 2 epithelial cells,express alveolar surfactant protein.However,compared with typical Alveolar type 2 epithelial cells AT2,the expression of active antibacterial substances decreased.As the first effector cell of coal dust phagocytosis,macrophages also showed apparent heterogeneity.9-months after coal dust exposure,the number of macrophages increased and polarized to M2,playing the role of anti-inflammatory and promoting repair.CD206 and MLPH double-positive cells were identified as a unique coal dust-induced M2 macrophage subgroup but significantly reduced after vitamin D supplementation.This study provides evidence for the correlation between vitamin D deficiency and poor lung function in workers exposed to coal dust.Biomarkers of early lung injury after coal dust exposure were screened.Single-cell sequencing analysis revealed changes in lung epithelial and macrophage lineage heterogeneity after coal dust exposure.Transcriptome data analysis identified cellular and molecular mechanisms of inflammation and fibrosis induced by long-term coal dust exposure and found a potential target of vitamin D in coal pneumoconiosis.In short,this study provides a scientific basis for vitamin D as good prevention and treatment for coal pneumoconiosis.Fig.[78]table[18]reference[349]... |
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