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Journal of Hazardous Materials Jan 2024Macrophages are essential for the maintenance of endothelial cell function. However, the potential impact and mechanisms of crosstalk between macrophages and endothelial...
Macrophages are essential for the maintenance of endothelial cell function. However, the potential impact and mechanisms of crosstalk between macrophages and endothelial cells during silicosis progression remain unexplored. To fill this knowledge gap, a mouse model of silicosis was established. Single cell sequencing, spatial transcriptome sequencing, western blotting, immunofluorescence staining, tube-forming and wound healing assays were used to explore the effects of silicon dioxide on macrophage-endothelial interactions. To investigate the mechanism of macrophage-mediated fibrosis, MMP12 was specifically inactivated using siRNA and pharmacological approaches, and macrophages were depleted using disodium chlorophosphite liposomes. Compared to the normal saline group, the silica dust group showed altered macrophage-endothelial interactions. Matrix metalloproteinase family member MMP12 was identified as a key mediator of the altered function of macrophage-endothelial interactions after silica exposure, which was accompanied by pro-inflammatory macrophage activation and fibrotic progression. By using ablation strategies, macrophage-derived MMP12 was shown to mediate endothelial cell dysfunction by accumulating on the extracellular matrix. During the inflammatory phase of silicosis, MMP12 secreted by pro-inflammatory macrophages caused decreased endothelial cell viability, reduced migration, decreased trans-endothelial resistance and increased permeability; while during the fibrotic phase, macrophage-derived MMP12 sustained endothelial cell injury through accumulation on the extracellular matrix.
Topics: Animals; Mice; Matrix Metalloproteinase 12; Endothelial Cells; Fibrosis; Macrophages; Silicosis; Silicon Dioxide
PubMed: 37816293
DOI: 10.1016/j.jhazmat.2023.132733 -
Current Opinion in Allergy and Clinical... Apr 2024There is a well established association between silica inhalational exposure and autoimmune disease, particularly in the context of intense exposure. We will provide in... (Review)
Review
PURPOSE OF REVIEW
There is a well established association between silica inhalational exposure and autoimmune disease, particularly in the context of intense exposure. We will provide in this article an update overview of new sources of silica dust exposure, with evidences of mechanisms from human and animal studies for association between silica and autoimmune diseases, their early detection of silicosis and new options for treatment.
RECENT FINDINGS
New industries such as jewelry polishing, denim jean production, fabrication of artificial stone benchtops, glass manufacturing and glassware has led to re-emergence of silicosis around the world. Silicosis with long term exposure to dust containing crystalline silica has been examined as a possible risk factor with respect to several autoimmune diseases as scleroderma, rheumatoid arthritis, lupus erythematosus, and some types of small vessel vasculitis with renal involvement. The dust may act to promote or accelerate disease development, requiring some other factors to break immune tolerance or initiate autoimmunity. Autophagy, apoptosis, or pyroptosis-related signaling pathways have also been suggested to contribute to the formation of those pathways with coordination of environmental co-exposure that can magnify autoimmune vulnerability.
SUMMARY
Better understanding the mechanisms that involve silica -induced autoimmune diseases may contribute to early diagnosis.
Topics: Animals; Humans; Occupational Exposure; Silicosis; Silicon Dioxide; Autoimmune Diseases; Dust
PubMed: 38277164
DOI: 10.1097/ACI.0000000000000966 -
CMAJ : Canadian Medical Association... Feb 2024
Topics: Humans; Middle Aged; Berylliosis; Metal Workers
PubMed: 38346777
DOI: 10.1503/cmaj.221680-f -
The International Journal of... Nov 2023Respiratory diseases of infectious, allergic, neoplastic or degenerative origin are due to the interaction of environmental and occupational risk factors, individual...
Respiratory diseases of infectious, allergic, neoplastic or degenerative origin are due to the interaction of environmental and occupational risk factors, individual susceptibility and other co-factors and comorbidities. Asthma and other respiratory pathologies can be worsened by climate change and exposure to other agents in occupational environments. PubMed and Scopus, and several websites on public and occupational health were queried to find publications and documents on work-related respiratory diseases, asthma, rhinitis, chronic obstructive pulmonary disease (COPD), pneumoconiosis and allergic alveolitis in association with climate change. Most of the retrieved articles concerned asthma (75 in Scopus), while the other topics were less frequently covered in the scientific literature, with a maximum of 29 papers for rhinitis and 23 for COPD. The most important terms highlighted by the word clouds were 'health', 'air', 'pollution', and, only for asthma and rhinitis, 'pollen' and 'allergic/allergy'. Website data on public and occupational health, and climate change were reported. Assessment and management of respiratory diseases that recognise occupational exposures should be improved, and more research into integrated approaches should be favoured. Health surveillance practices for workers exposed to agents that cause respiratory diseases should be implemented. The development of biomarkers of exposure, effect and susceptibility needs further study.
Topics: Humans; Rhinitis; Climate Change; Asthma; Hypersensitivity; Respiration Disorders; Occupational Diseases; Occupational Exposure; Pulmonary Disease, Chronic Obstructive; Respiratory Tract Diseases
PubMed: 37880894
DOI: 10.5588/ijtld.23.0131 -
Biomedicines Dec 2023Club cells have a distinct role in the epithelial repair and defense mechanisms of the lung. After exposure to environmental pollutants, during chronic exposure, the... (Review)
Review
Club cells have a distinct role in the epithelial repair and defense mechanisms of the lung. After exposure to environmental pollutants, during chronic exposure, the secretion of club cells secretory protein (CCSP) decreases. Exposure to occupational hazards certainly has a role in a large number of interstitial lung diseases. According to the American Thoracic Society and the European Respiratory Society, around 40% of the all interstitial lung disease is attributed to occupational hazards. Some of them are very well characterized (pneumoconiosis, hypersensitivity pneumonitis), whereas others are consequences of acute exposure (e.g., paraquat) or persistent exposure (e.g., isocyanate). The category of vapors, gases, dusts, and fumes (VGDF) has been proven to produce subclinical modifications. The inflammation and altered repair process resulting from the exposure to occupational respiratory hazards create vicious loops of cooperation between epithelial cells, mesenchymal cells, innate defense mechanisms, and immune cells. The secretions of club cells modulate the communication between macrophages, epithelial cells, and fibroblasts mitigating the inflammation and/or reducing the fibrotic process. In this review, we describe the mechanisms by which club cells contribute to the development of interstitial lung diseases and the potential role for club cells as biomarkers for occupational-related fibrosis.
PubMed: 38255185
DOI: 10.3390/biomedicines12010078 -
Korean Journal of Radiology Aug 2023Occupational lung diseases (OLD) are a group of preventable conditions caused by noxious inhalation exposure in the workplace. Workers in various industries are at a... (Review)
Review
Occupational lung diseases (OLD) are a group of preventable conditions caused by noxious inhalation exposure in the workplace. Workers in various industries are at a higher risk of developing OLD. Despite regulations contributing to a decreased incidence, OLD remain among the most frequently diagnosed work-related conditions, contributing to significant morbidity and mortality. A multidisciplinary discussion (MDD) is necessary for a timely diagnosis. Imaging, particularly computed tomography, plays a central role in diagnosing OLD and excluding other inhalational lung diseases. OLD can be broadly classified into fibrotic and non-fibrotic forms. Imaging reflects variable degrees of inflammation and fibrosis involving the airways, parenchyma, and pleura. Common manifestations include classical pneumoconioses, chronic granulomatous diseases (CGD), and small and large airway diseases. Imaging is influenced by the type of inciting exposure. The findings of airway disease may be subtle or solely uncovered upon expiration. High-resolution chest CT, including expiratory-phase imaging, should be performed in all patients with suspected OLD. Radiologists should familiarize themselves with these imaging features to improve diagnostic accuracy.
Topics: Humans; Lung Diseases; Pneumoconiosis; Occupational Diseases; Tomography, X-Ray Computed; Occupational Exposure
PubMed: 37500580
DOI: 10.3348/kjr.2023.0274 -
Pulmonology Jun 2023Silicosis mostly happens in workers with high silica exposure and may accompany the development of various diseases like tuberculosis, cancer, or autoimmune diseases.... (Review)
Review
INTRODUCTION
Silicosis mostly happens in workers with high silica exposure and may accompany the development of various diseases like tuberculosis, cancer, or autoimmune diseases. The term silico-tuberculosis describes a condition in which an individual is affected by both silicosis and tuberculosis at the same time. This systematic review and meta-analysis study was conducted to evaluate the risk of tuberculosis in silicosis patients and individuals exposed to silica dust.
METHODS
We performed a systematic search for relevant studies up to 6 September 2022 using PubMed/ Medline, and Embase with the following keywords in titles or abstracts: "silicosis" OR "silicoses" OR "pneumoconiosis" OR "pneumoconioses" AND "tuberculosis". Cohort and case-control studies containing relevant and original information about tuberculosis infection in silicosis patients were included for further analysis. Pooled estimates and 95% confidence intervals (CI) for the relative risk of tuberculosis in individuals with silicosis compared to those without; these were evaluated using the random effects model due to the estimated heterogeneity of the true effect sizes.
RESULTS
Out of 5352 potentially relevant articles, 7 studies were eligible for systematic review, of which 4 cohort studies were included for meta-analysis. The total population of all studies was 5884, and 90.63% were male. The mean age of participants was 47.7 years. Our meta-analysis revealed a pooled risk ratio of 1.35 (95%CI 1.18-1.53, I : 94.30%) which means an increased risk of silicosis patients and silica-exposed individuals to tuberculosis infection.
CONCLUSION
Silicosis and silica dust exposure increase the risk of tuberculosis. Therefore, we suggest that individuals with long-time silica exposure, like mine workers, be routinely considered for both silicosis and tuberculosis screening programs.
PubMed: 37349198
DOI: 10.1016/j.pulmoe.2023.05.001