Nicotine exposure exacerbates silica-induced pulmonary fibrosis via STAT3-BDNF-TrkB-mediated epithelial-mesenchymal transition in alveolar type II cells

Chen, Haoming; Tao, Xinrong; Cao, Hangbing; Li, Bing; Sun, Qi; Wang, Qianqian; Zou, Yuanjie; Mu, Min; Tao, Huihui; Zhao, Yehong; Ge, Deyong

doi:10.1016/j.fct.2023.113694

Cited by 4 publications

(2 citation statements)

References 58 publications

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“…It is well-known that the duration of silica exposure is an important factor in the development of silicosis ( 1 , 5 ) because exposure duration reflects, to some extent, the cumulative dose of silica ( 1 ). As for smoking history, recent animal experimental data have shown that smoking can aggravate inflammation and pulmonary fibrosis of silicosis ( 31 , 32 ). The findings from these animal studies suggest that cigarette smoking may be associated with the severity of silicosis, thereby supporting our study results.…”

Section: Discussionmentioning

confidence: 99%

The systemic immune-inflammation index is significantly associated with the severity of silicosis: a 9-year retrospective study in Beijing

Kang,

Cao,

Shao

et al. 2024

Front. Med.

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BackgroundSilicosis shows an increasing trend with the development of new industries. However, the potential biomarkers for predicting the disease severity are lacking. A novel inflammatory marker, the systemic immune-inflammation Index (SII), has not been studied in silicosis.MethodsIn this retrospective study, we used data from a big database platform of a tertiary general hospital in Beijing, which was established based on the electronic medical records of the hospital. The clinical data of adult patients diagnosed with silicosis at the Department of Occupational Medicine and Toxicology from 2013 to 2022 were collected. The data extracted from the database were in de-identified form. Only patients with a first diagnosis of silicosis and without conditions that might affect the parameters of routine blood tests were included in the analysis. Analyses were performed to assess the relationship between SII and the advanced stage of silicosis.ResultsA total of 246 participants were included in the study. Most of the patients were exposed to silica particles during excavation and digging (n = 149, 60.6%). SII level was significantly higher in patients with advanced stages of silicosis. A multivariate logistic regression analysis revealed that a higher SII level was associated with the advanced stage of silicosis [odds ratio (OR) = 1.002; 95% confidence interval (CI): 1.000–1.003, p < 0.001] after adjusting for all covariates. The best cutoff value of SII was 444.1. The results of the subgroup analysis also showed a significant correlation between SII level over 444.1 and the advanced stage of silicosis in groups stratified by gender, history of smoking, and duration of silica exposure. Moreover, our results showed a significant but weak negative correlation between the level of SII and some lung function parameters in silicosis.ConclusionHigher SII is associated with the advanced stage of silicosis and impaired lung function. More long-term, large-scale studies are needed to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

The systemic immune-inflammation index is significantly associated with the severity of silicosis: a 9-year retrospective study in Beijing

Kang,

Cao,

Shao

et al. 2024

Front. Med.

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“…To simulate the chronic exposure encountered by workers, the experimental animals were subjected to multiple nasal instillations of silica suspension 30 . Our previous study observed that mice exposed to coal dust repeatedly on multiple occasions exhibited a significant decrease in mobility and physical activity during the OFT after 28 days 31 .…”

Section: Discussionmentioning

confidence: 99%

Nicotine suppresses crystalline silica‐induced astrocyte activation and neuronal death by inhibiting NF‐κB in the mouse hippocampus

Cao,

Li,

et al. 2023

CNS Neurosci Ther

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AimsExposure to crystalline silica (CS) in occupational settings induces chronic inflammation in the respiratory system and, potentially, the brain. Some workers are frequently concurrently exposed to both CS and nicotine. Here, we explored the impact of nicotine on CS‐induced neuroinflammation in the mouse hippocampus.MethodsIn this study, we established double‐exposed models of CS and nicotine in C57BL/6 mice. To assess depression‐like behavior, experiments were conducted at 3, 6, and 9 weeks. Serum inflammatory factors were analyzed by ELISA. Hippocampus was collected for RNA sequencing analysis and examining the gene expression patterns linked to inflammation and cell death. Microglia and astrocyte activation and hippocampal neuronal death were assessed using immunohistochemistry and immunofluorescence staining. Western blotting was used to analyze the NF‐κB expression level.ResultsMice exposed to CS for 3 weeks showed signs of depression. This was accompanied by elevated IL‐6 in blood, destruction of the blood–brain barrier, and activation of astrocytes caused by an increased NF‐κB expression in the CA1 area of the hippocampus. The elevated levels of astrocyte‐derived Lcn2 and upregulated genes related to inflammation led to higher neuronal mortality. Moreover, nicotine mitigated the NF‐κB expression, astrocyte activation, and neuronal death, thereby ameliorating the associated symptoms.ConclusionSilica exposure induces neuroinflammation and neuronal death in the mouse hippocampal CA1 region and depressive behavior. However, nicotine inhibits CS‐induced neuroinflammation and neuronal apoptosis, alleviating depressive‐like behaviors in mice.

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2-Deoxy-D-glucose ameliorates inflammation and fibrosis in a silicosis mouse model by inhibiting hypoxia-inducible factor-1α in alveolar macrophages

Lu,

Mu,

RenChen

et al. 2024

Ecotoxicology and Environmental Safety

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Nicotine exposure exacerbates silica-induced pulmonary fibrosis via STAT3-BDNF-TrkB-mediated epithelial-mesenchymal transition in alveolar type II cells

Cited by 4 publications

References 58 publications

The systemic immune-inflammation index is significantly associated with the severity of silicosis: a 9-year retrospective study in Beijing

The systemic immune-inflammation index is significantly associated with the severity of silicosis: a 9-year retrospective study in Beijing

Nicotine suppresses crystalline silica‐induced astrocyte activation and neuronal death by inhibiting NF‐κB in the mouse hippocampus

2-Deoxy-D-glucose ameliorates inflammation and fibrosis in a silicosis mouse model by inhibiting hypoxia-inducible factor-1α in alveolar macrophages

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