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Frontiers in Public Health 2024To investigate the causal relationships between pneumoconiosis and rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and gout.
OBJECTIVES
To investigate the causal relationships between pneumoconiosis and rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and gout.
METHODS
The random-effects inverse variance weighted (IVW) approach was utilized to explore the causal effects of the instrumental variables (IVs). Sensitivity analyses using the MR-Egger and weighted median (WM) methods were did to investigate horizontal pleiotropy. A leave-one-out analysis was used to avoid the bias resulting from single-nucleotide polymorphisms (SNPs).
RESULTS
There was no causal association between pneumoconiosis and SLE, RA or gout in the European population [OR = 1.01, 95% CI: 0.94-1.10, = 0.74; OR = 1.00, 95% CI: 0.999-1.000, = 0.50; OR = 1.00, 95% CI: 1.000-1.001, = 0.55]. Causal relationships were also not found in pneumoconiosis due to asbestos and other mineral fibers and SLE, RA and gout [OR = 1.01, 95% CI: 0.96-1.07, = 0.66; OR = 1.00, 95% CI: 1.00-1.00, = 0.68; OR = 1.00, 95% CI: 1.00-1.00, = 0.20].
CONCLUSION
Our study suggests that pneumoconiosis may have no causal relationship with the three inflammatory immune diseases.
Topics: Humans; Mendelian Randomization Analysis; Pneumoconiosis; Gout; Immune System Diseases; Lupus Erythematosus, Systemic
PubMed: 38601492
DOI: 10.3389/fpubh.2024.1373044 -
Respirology (Carlton, Vic.) Jul 2024Air pollutants have various effects on human health in environmental and occupational settings. Air pollutants can be a risk factor for incidence,... (Review)
Review
Air pollutants have various effects on human health in environmental and occupational settings. Air pollutants can be a risk factor for incidence, exacerbation/aggravation and death due to various lung diseases, including asthma, chronic obstructive pulmonary disease (COPD), hypersensitivity pneumonitis or pneumonia (HP), pulmonary fibrosis such as pneumoconiosis and malignant respiratory diseases such as lung cancer and malignant pleural mesothelioma. Environmental and occupational respiratory diseases are crucial clinical and social issues worldwide, although the burden of respiratory disease due to environmental and occupational causes varies depending on country/region, demographic variables, geographical location, industrial structure and socioeconomic situation. The correct recognition of environmental and occupational lung diseases and taking appropriate measures are essential to their effective prevention.
Topics: Humans; Occupational Diseases; Lung Diseases; Occupational Exposure; Environmental Exposure; Risk Factors; Air Pollutants; Lung Neoplasms; Pulmonary Disease, Chronic Obstructive
PubMed: 38826078
DOI: 10.1111/resp.14761 -
China CDC Weekly Sep 2023Pneumoconiosis, recognized as one of the most detrimental occupational diseases in China, exhibits a multimorbidity profile due to a plethora of comorbidities and...
WHAT IS ALREADY KNOWN ABOUT THIS TOPIC?
Pneumoconiosis, recognized as one of the most detrimental occupational diseases in China, exhibits a multimorbidity profile due to a plethora of comorbidities and complications. These factors significantly influence the treatment outcomes, progression, prognosis, and overall quality of life of the afflicted patients.
WHAT IS ADDED BY THIS REPORT?
The present study examined the prevalence and types of comorbidities, encompassing 13 common diseases or conditions, within cases of pneumoconiosis across 27 provincial-level administrative divisions (PLADs) in China. Distinctions in multimorbidity distribution by gender, urban . rural areas, stages of pneumoconiosis, and the smoking index were considered. Furthermore, the study investigated the patterns of multimorbidity.
WHAT ARE THE IMPLICATIONS FOR PUBLIC HEALTH PRACTICE?
This study serves as a reference point for the formulation of treatment strategies and health policy development concerning pneumoconiosis in China.
PubMed: 37814646
DOI: 10.46234/ccdcw2023.159 -
BMC Cancer Nov 2023Ankyrin repeat domain 49 (ANKRD49) has been found to be highly expressed in multiple cancer including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC)....
BACKGROUND
Ankyrin repeat domain 49 (ANKRD49) has been found to be highly expressed in multiple cancer including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). However, the function of ANKRD49 in the pathogenesis of NSCLC still remains elusive. Previously, ANKRD49 has been demonstrated to promote the invasion and metastasis of A549 cells, a LUAD cell line, via activating the p38-ATF-2-MMP2/MMP9 pathways. Considering the heterogeneity of tumor cells, the function and mechanism of ANKRD49 in NSCLC need more NSCLC-originated cells to clarify.
METHODS
Real-time qPCR was employed to test ANKRD49 expression levels in nine pairs of fresh NSCLC tissues and the corresponding adjacent normal tissues. The function of ANKRD49 was investigated using overexpression and RNA interference assays in lung adenocarcinoma cell line (NCI-H1299) and lung squamous carcinoma cell line (NCI-H1703) through gelatin zymography, cell counting kit-8, colony formation, wound healing, migration and invasion assays mmunoprecipitation was performed to in vitro. Immunoprecipitation was performed to test the interaction of c-Jun and ATF2. Chromatin immunoprecipitation was conducted to assess the transcriptional regulation of ATF2/c-Jun on MMP-2/9. Moreover, the tumorigenicity of ANKRD49 was evaluated in nude mice models and the involved signal molecular was also measured by immunohistochemical method.
RESULTS
We found that the levels of ANKRD49 in cancerous tissues were higher than those in adjacent normal tissues. in vitro assay showed that ANKRD49 promoted the migration and invasion of NCI-H1299 and NCI-H1703 cells via enhancing the levels of MMP-2 and MMP-9. Furthermore, ANKRD49 elevated phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2:c-Jun with the promoter MMP-2 or MMP-9. In vivo assay showed that ANKRD49 promoted lung metastasis of injected-NSCLC cells and the high metastatic rate was positively correlated with the high expression of ANKRD49, MMP-2, MMP-9, p-JNK, p-c-Jun and p-ATF2.
CONCLUSION
The present study indicated that ANKRD49 accelerated the invasion and metastasis of NSCLC cells via JNK-mediated transcription activation of c-Jun and ATF2 which regulated the expression of MMP-2/MMP-9. The molecular mechanisms of ANKRD49's function is different from those found in A549 cells. The current study is a supplement and improvement to the previous research.
Topics: Animals; Mice; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Mice, Nude; Cell Proliferation; Cell Line, Tumor; Carcinoma, Non-Small-Cell Lung; Lung Neoplasms; Carcinoma, Squamous Cell; Adenocarcinoma of Lung
PubMed: 37964204
DOI: 10.1186/s12885-023-11612-9 -
Ecotoxicology and Environmental Safety Dec 2023Macrophage pyroptosis has recently been involved in some inflammatory and fibrosis diseases, however, the role of macrophage pyroptosis in silica-induced pulmonary...
Macrophage pyroptosis has recently been involved in some inflammatory and fibrosis diseases, however, the role of macrophage pyroptosis in silica-induced pulmonary fibrosis has not been fully elucidated. In this study, we explored the role of macrophage pyroptosis in silicosis in vivo and in vitro. A mouse model of silicosis was established and mice were sacrificed at 7, 14, and 28 days after exposure of silica. The results revealed that the expression of GSDMD and other pyroptosis-related indicators was up-regulated obviously at 14 days after silica exposure, indicating that silica induced pyroptosis in vivo. In vitro, human monocytic leukemia cells (THP-1) and human lung fibroblasts (MRC-5) were used to detect the relationship between macrophage pyroptosis and lung fibroblasts. It showed that silica increased the levels of GSDMD and other pyroptosis-related indicators remarkably in macrophages and the supernatant of macrophage stimulated by silica could promote the upregulation of fibrosis markers in fibroblasts. However, GSDMD knockdown suppressed silica-induced macrophage pyroptosis and alleviated the upregulation of fibrosis markers in fibroblasts, suggesting the important role of macrophage pyroptosis in the activation of myofibroblasts during the progression of silicosis. Taken together, it showed that silica could induce macrophage pyroptosis and inhibiting macrophage pyroptosis could be a feasible clinical strategy to alleviate silicosis.
Topics: Mice; Humans; Animals; Pulmonary Fibrosis; Silicon Dioxide; Pyroptosis; Macrophages; Silicosis; Fibrosis
PubMed: 37976936
DOI: 10.1016/j.ecoenv.2023.115693 -
Cellular Signalling Aug 2023Silicosis is a progressive and irreversible common occupational disease caused by long-term inhalation of a large amount of free silica dust. Its pathogenesis is...
Silicosis is a progressive and irreversible common occupational disease caused by long-term inhalation of a large amount of free silica dust. Its pathogenesis is complex, and the existing prevention and treatment methods can not effectively improve silicosis injury. To uncover potential differential genes in silicosis, SiO-stimulated rats and their control original transcriptomic data sets GSE49144, GSE32147 and GSE30178 were downloaded for further bioinformatics analysis. We used R packages to extract and standardize transcriptome profiles, then screened differential genes, and enriched GO and KEGG pathways through clusterProfiler packages. In addition, we investigated the role of lipid metabolism in the progression of silicosis by qRT-PCR validation and transfection with si-CD36. A total of 426 differential genes were identified in this study. Based on GO and KEGG enrichment analysis, it was found that lipid and atherosclerosis were significantly enriched. qRT-PCR was used to detect the relative expression level of differential genes in this signaling pathway of silicosis rat models. mRNA levels of Abcg1, Il1b, Sod2, Cyba, Cd14, Cxcl2, Ccl3, Cxcl1, Ccl2 and CD36 increased, mRNA levels of Ccl5, Cybb and Il18 decreased. In addition, at the cellular level, SiO-stimulated lead to lipid metabolism disorder in NR8383, and silencing CD36 inhibited SiO-induced lipid metabolism disorder. These results indicate that lipid metabolism plays an important role in the progression of silicosis, and the genes and pathways reported in this study may provide new ideas for the pathogenesis of silicosis.
Topics: Rats; Animals; Silicon Dioxide; Lipid Metabolism; Silicosis; Gene Expression Profiling; RNA, Messenger; NADPH Oxidase 2
PubMed: 37224986
DOI: 10.1016/j.cellsig.2023.110716 -
China CDC Weekly Oct 2023
Review
PubMed: 37970069
DOI: 10.46234/ccdcw2023.162 -
International Journal of Biological... 2023Silicosis is a common and ultimately fatal occupational disease, yet the limited therapeutic option remains the major clinical challenge. Apelin, an endogenous ligand of...
Silicosis is a common and ultimately fatal occupational disease, yet the limited therapeutic option remains the major clinical challenge. Apelin, an endogenous ligand of the G-protein-coupled receptor (APJ), is abundantly expressed in diverse organs. The apelin-APJ axis helps to control pathological and physiological processes in lung. The role of apelin in the pathological process and its possible therapeutic effects on silicosis have not been elucidated. In this study, we found that lung expression and circulating levels of apelin were markedly decreased in silicosis patients and silica-induced fibrotic mice and associated with the severity. Furthermore, data demonstrated that pre-treatment from day 3 and post-treatment from day 15 with apelin could both alleviate silica-induced pulmonary fibrosis in mice. Besides, apelin inhibited pulmonary fibroblast activation via transforming growth factor beta 1 (TGF-β1) signaling. Our study suggested that apelin could prevent and reverse silica-induced pulmonary fibrosis by inhibiting the fibroblast activation through TGF-β1 signaling pathway, thus providing a new potential therapeutic strategy for silicosis and other pulmonary fibrosis.
Topics: Animals; Mice; Apelin; Fibroblasts; Pulmonary Fibrosis; Silicon Dioxide; Silicosis; Transforming Growth Factor beta1
PubMed: 37705751
DOI: 10.7150/ijbs.81436 -
CMAJ : Canadian Medical Association... Dec 2023
Topics: Humans; Middle Aged; Berylliosis; Metal Workers
PubMed: 38049163
DOI: 10.1503/cmaj.221680 -
Frontiers in Cellular and Infection... 2023Pneumoconiosis patients have a high prevalence of pulmonary infections, which can complicate diagnosis and treatment. And there is no comprehensive study of the...
BACKGROUND
Pneumoconiosis patients have a high prevalence of pulmonary infections, which can complicate diagnosis and treatment. And there is no comprehensive study of the microbiome of patients with pneumoconiosis. The application of metagenomic next-generation sequencing (mNGS) fills the gap to some extent by analyzing the lung microbiota of pneumoconiosis population while achieving accurate diagnosis.
METHODS
We retrospectively analyzed 44 patients with suspected pneumoconiosis complicated with pulmonary infection between Jan 2020 and Nov 2022. Bronchoalveolar lavage fluid (BALF) specimens from 44 patients were collected and tested using the mNGS technology.
RESULTS
Among the lung microbiome of pneumoconiosis patients with complicated pulmonary infection (P group), the most frequently detected bacteria and fungi at the genus level were and , at the species level were and , respectively, and the most frequently detected DNA virus was . There was no significant difference in α diversity between the P group and the non-pneumoconiosis patients complicated with pulmonary infection group (Non-P group) in pulmonary flora, while 0.01 for β diversity analysis, and the differential species between the two groups were and . In addition, we monitored a high distribution of and in the P group, while herpes virus was detected in the majority of samples.
CONCLUSIONS
Overall, we not only revealed a comprehensive lung microbiome profile of pneumoconiosis patients, but also compared the differences between their microbiome and that of non-pneumoconiosis complicated with pulmonary infection patients. This provides a good basis for a better understanding of the relationship between pneumoconiosis and microorganisms, and for the search of potential biomarkers.
Topics: Humans; Retrospective Studies; Pneumonia; Microbiota; High-Throughput Nucleotide Sequencing; Biomarkers; Lung; Sensitivity and Specificity; Metagenomics
PubMed: 37545858
DOI: 10.3389/fcimb.2023.1200157