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Journal of Clinical Tuberculosis and... May 2021Silicosis continues to be a serious health issue in many countries and its elimination by 2030 (a target set by WHO and the International Labour Organization in 1995) is... (Review)
Review
Silicosis continues to be a serious health issue in many countries and its elimination by 2030 (a target set by WHO and the International Labour Organization in 1995) is virtually impossible. The risk to develop pulmonary tuberculosis for silicosis patients is higher than for non-silicosis people, and there is also an increased risk of both pulmonary and extrapulmonary tuberculosis in individuals exposed to silica. HIV coinfection adds further to the risk, and in some countries, such as South Africa, miners living with HIV are a considerable number. The diagnosis of active tuberculosis superimposed on silicosis is often problematic, especially in initial phases, and chest X-ray and smear examination are particularly important for the diagnosis of pulmonary tuberculosis. Treatment is difficult; directly observed therapy is recommended, a duration of at least eight months is probably needed, drug reactions are frequent and the risk of relapse higher than in non-silicosis patients. TB prevention in silicosis patients is essential and include active surveillance of the workers, periodic chest X-rays, tuberculin skin test or interferon-gamma releasing assay testing, and, importantly, adoption of measures to reduce the exposure to silica dust. Chemoprophylaxis is possible with different regimens and needs to be expanded around the world, but efficacy is unfortunately limited. Silico-tuberculosis is still a challenging health problem in many countries and deserves attention worldwide.
PubMed: 33598569
DOI: 10.1016/j.jctube.2021.100218 -
The European Respiratory Journal Dec 2015Latent tuberculosis infection (LTBI) is characterised by the presence of immune responses to previously acquired Mycobacterium tuberculosis infection without clinical... (Review)
Review
Latent tuberculosis infection (LTBI) is characterised by the presence of immune responses to previously acquired Mycobacterium tuberculosis infection without clinical evidence of active tuberculosis (TB). Here we report evidence-based guidelines from the World Health Organization for a public health approach to the management of LTBI in high risk individuals in countries with high or middle upper income and TB incidence of <100 per 100 000 per year. The guidelines strongly recommend systematic testing and treatment of LTBI in people living with HIV, adult and child contacts of pulmonary TB cases, patients initiating anti-tumour necrosis factor treatment, patients receiving dialysis, patients preparing for organ or haematological transplantation, and patients with silicosis. In prisoners, healthcare workers, immigrants from high TB burden countries, homeless persons and illicit drug users, systematic testing and treatment of LTBI is conditionally recommended, according to TB epidemiology and resource availability. Either commercial interferon-gamma release assays or Mantoux tuberculin skin testing could be used to test for LTBI. Chest radiography should be performed before LTBI treatment to rule out active TB disease. Recommended treatment regimens for LTBI include: 6 or 9 month isoniazid; 12 week rifapentine plus isoniazid; 3-4 month isoniazid plus rifampicin; or 3-4 month rifampicin alone.
Topics: Antirheumatic Agents; Antitubercular Agents; Coinfection; Comorbidity; Disease Management; Drug Users; Emigrants and Immigrants; Evidence-Based Medicine; HIV Infections; Health Personnel; Ill-Housed Persons; Humans; Interferon-gamma Release Tests; Isoniazid; Kidney Failure, Chronic; Latent Tuberculosis; Mass Screening; Practice Guidelines as Topic; Prisoners; Public Health; Radiography, Thoracic; Renal Dialysis; Rifampin; Risk Assessment; Silicosis; Substance-Related Disorders; Transplant Recipients; Tuberculin Test; Tumor Necrosis Factor-alpha; World Health Organization
PubMed: 26405286
DOI: 10.1183/13993003.01245-2015 -
Acta Pharmaceutica Sinica. B Mar 2022Silicosis is a leading cause of occupational disease-related morbidity and mortality worldwide, but the molecular basis underlying its development remains unclear. An...
Silicosis is a leading cause of occupational disease-related morbidity and mortality worldwide, but the molecular basis underlying its development remains unclear. An accumulating body of evidence supports gasdermin D (GSDMD)-mediated pyroptosis as a key component in the development of various pulmonary diseases. However, there is little experimental evidence connecting silicosis and GSDMD-driven pyroptosis. In this work, we investigated the role of GSDMD-mediated pyroptosis in silicosis. Single-cell RNA sequencing of healthy and silicosis human and murine lung tissues indicated that GSDMD-induced pyroptosis in macrophages was relevant to silicosis progression. Through microscopy we then observed morphological alterations of pyroptosis in macrophages treated with silica. Measurement of interleukin-1 release, lactic dehydrogenase activity, and real-time propidium iodide staining further revealed that silica induced pyroptosis of macrophages. Additionally, we verified that both canonical (caspase-1-mediated) and non-canonical (caspase-4/5/11-mediated) signaling pathways mediated silica-induced pyroptosis activation, and . Notably, knockout mice exhibited dramatically alleviated silicosis phenotypes, which highlighted the pivotal role of pyroptosis in this disease. Taken together, our results demonstrated that macrophages underwent GSDMD-dependent pyroptosis in silicosis and inhibition of this process could serve as a viable clinical strategy for mitigating silicosis.
PubMed: 35530143
DOI: 10.1016/j.apsb.2021.10.006 -
Ecotoxicology and Environmental Safety Oct 2022Macrophages play an important role in causing silicosis eventually becoming an irreversible fibrotic disease, and there are no specific drugs for silicosis in the clinic...
Macrophages play an important role in causing silicosis eventually becoming an irreversible fibrotic disease, and there are no specific drugs for silicosis in the clinic so far. Pirfenidone has consistently been shown to have anti-inflammatory and anti-fibrotic effects, but the specific mechanism by which it ameliorates fibrosis in silicosis is unclear. A rat silicosis model was established in this study, and lung tissues and serum were collected by batch execution at 14, 28, and 56 days. Also, the effects of Pirfenidone on macrophage polarization and pulmonary fibrosis were evaluated in silicosis with early intervention and late treatment by histological examination, Enzyme-linked immunosorbent assay, Hydroxyproline assay, Western blot and Quantitative reverse transcription polymerase chain reaction. The results showed that Pirfenidone significantly reduced pulmonary fibrosis in rats with silicosis, and both early intervention and late treatment effectively inhibited the expression of α-SMA, Col-I, Vimentin, Hydroxyproline, IL-1β, IL-18, and the M2 macrophage marker CD206 and Arg-1, while only early intervention effectively inhibited E-cad, TGF-β1, TNF-α, and the M1 macrophage marker iNOS, CD86. Furthermore, Pirfenidone dramatically reduced the mRNA expression of the JAK2/STAT3. These findings imply that Pirfenidone may reduce pulmonary fibrosis in silicosis rats by inhibiting macrophage polarization via the JAK2/STAT3 signaling pathway.
Topics: Animals; Fibrosis; Hydroxyproline; Interleukin-18; Janus Kinase 2; Macrophages; Pneumonia; Pulmonary Fibrosis; Pyridones; RNA, Messenger; Rats; Signal Transduction; Silicosis; Transforming Growth Factor beta1; Tumor Necrosis Factor-alpha; Vimentin
PubMed: 36108436
DOI: 10.1016/j.ecoenv.2022.114066 -
International Journal of Occupational... Oct 2018The correlation between quartz dust concentrations in the Swiss enterprises and the incidence of silicosis and other related diseases acknowledged as occupational...
OBJECTIVES
The correlation between quartz dust concentrations in the Swiss enterprises and the incidence of silicosis and other related diseases acknowledged as occupational diseases (OD) was investigated.
MATERIAL AND METHODS
Quartz dust concentrations were obtained from Suva's databases of occupational health surveillance measurements between 2005 and 2014. Information on quartz dust-related diseases was from medical dossiers of workers with OD acknowledged by Suva between 2005 and 2014.
RESULTS
The median quartz dust concentration of the 2579 measurements between 2005 and 2014 was 0.09 mg/m (alveolar fraction). Out of all measurements, 28% were above the Swiss occupational exposure limit (OEL) of 0.15 mg/m (alveolar fraction). One hundred eighty-one individuals suffered from acknowledged quartz dust-related disease (179 silicosis and 2 chronic obstructive pulmonary disease (COPD)). Additionally, 8 out of these workers were diagnosed with lung cancer and 55 with COPD of a non-specified cause. Out of all workers, 46% were exposed to silica dust for the first time before 1975 when the current Swiss OEL was introduced. Out of the foreign workers, 63% began to work abroad, during which they could have at least partly acquired their silicosis. Out of all workers, 75% were ever-smokers.
CONCLUSIONS
The incidence of silicosis decreased drastically from approximately 300 cases/year in the 1970s to fewer than 20 cases/year 20 years ago. Several findings of this study that could help to interpret the ongoing occurrence of the disease include excessive exposure in or outside of Switzerland in former or current times, vulnerability to the development of silicosis due to cigarette smoke, or poor compliance with wearing breathing masks. Int J Occup Med Environ Health 2018;31(5):659-676.
Topics: Adult; Aged; Air Pollutants, Occupational; Emigrants and Immigrants; Humans; Lung Neoplasms; Middle Aged; Occupational Exposure; Particulate Matter; Pulmonary Disease, Chronic Obstructive; Quartz; Silicosis; Smoking; Switzerland
PubMed: 30010160
DOI: 10.13075/ijomeh.1896.01272 -
Theranostics 2019Occupational exposure to crystalline silica (CS) particles leads to silicosis, which is characterized by chronic inflammation and abnormal tissue repair. Alveolar...
Occupational exposure to crystalline silica (CS) particles leads to silicosis, which is characterized by chronic inflammation and abnormal tissue repair. Alveolar macrophages (AMs) play a crucial role in the process of silicosis. Previously, we demonstrated positive effect of dioscin on silicosis through modulating macrophage-elicited innate immune response. However, the concrete molecular mechanism remains to be discovered. We established experimental model of silicosis with wildtype and Atg5Dppa3 mice and oral administrated dioscin daily to explore the effects of dioscin on macrophages and pulmonary fibrosis. AM cell line MH-S with Atg5 silence was used to explore specific function of dioscin on macrophage-derived inflammation and the underlying molecular mechanism. Dioscin could promote autophagy in macrophages. Dioscin-triggered AMs autophagy limited mitochondrial reactive oxygen species (mtROS) mass stimulated by CS, reduced mitochondria-dependent apoptosis pathway activation and facilitated cell survival. Relieved oxidative stress resulted in decreased secretion of inflammatory factors and chemokines. Dioscin treatment alleviated macrophage-derived inflammation and subsequent abnormal collagen repair. All the dioscin's protective effects were diminished in Atg5Dppa3 mice. Dioscin promoting autophagy leads to reduced CS-induced mitochondria-dependent apoptosis and cytokine production in AMs, which may provide concrete molecular mechanism for the therapy of silicosis.
Topics: Animals; Apoptosis; Autophagy; Cell Line; Cell Survival; Diosgenin; Female; Macrophages; Macrophages, Alveolar; Mice; Mice, Inbred C57BL; Mitochondria; Oxidative Stress; Pneumonia; Pulmonary Fibrosis; Reactive Oxygen Species; Silicon Dioxide; Silicosis
PubMed: 31037145
DOI: 10.7150/thno.29682 -
Nature Communications Oct 2015Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell...
Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization. Recent studies indicate that mitophagy and healthy mitochondrial function are critical to the survival of stem cells, but how these processes are regulated in MSCs is unknown. Here we show that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles. The vesicles are then engulfed and re-utilized via a process involving fusion by macrophages, resulting in enhanced bioenergetics. Furthermore, we show that MSCs simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling, thereby de-sensitizing macrophages to the ingested mitochondria. Collectively, these studies mechanistically link mitophagy and MSC survival with macrophage function, thereby providing a physiologically relevant context for the innate immunomodulatory activity of MSCs.
Topics: Animals; Arrestins; Blotting, Western; Cell-Derived Microparticles; Exosomes; Extracellular Vesicles; Flow Cytometry; Humans; Macrophages; Mesenchymal Stem Cells; Mice; MicroRNAs; Microscopy, Electron; Mitochondria; Mitophagy; Myeloid Differentiation Factor 88; Oxidative Stress; Receptors, Immunologic; Signal Transduction; Silicosis; Toll-Like Receptor 4; Toll-Like Receptor 9; Toll-Like Receptors
PubMed: 26442449
DOI: 10.1038/ncomms9472 -
Frontiers in Pharmacology 2024Silicosis is a chronic illness marked by diffuse fibrosis in lung tissue resulting from continuous exposure to SiO-rich dust in the workplace. The onset and progression... (Review)
Review
Silicosis is a chronic illness marked by diffuse fibrosis in lung tissue resulting from continuous exposure to SiO-rich dust in the workplace. The onset and progression of silicosis is a complicated and poorly understood pathological process involving numerous cells and molecules. However, silicosis poses a severe threat to public health in developing countries, where it is the most prevalent occupational disease. There is convincing evidence supporting that innate and adaptive immune cells, as well as their cytokines, play a significant role in the development of silicosis. In this review, we describe the roles of immune cells and cytokines in silicosis, and summarize current knowledge on several important inflammatory signaling pathways associated with the disease, aiming to provide novel targets and strategies for the treatment of silicosis-related inflammation.
PubMed: 38515835
DOI: 10.3389/fphar.2024.1362509 -
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 -
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