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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 -
Frontiers in Microbiology 2023Growing evidence indicates that variations in the composition of the gut microbiota are linked to the onset and progression of chronic respiratory diseases (CRDs),...
INTRODUCTION
Growing evidence indicates that variations in the composition of the gut microbiota are linked to the onset and progression of chronic respiratory diseases (CRDs), albeit the causal relationship between the two remains unclear.
METHODS
We conducted a comprehensive two-sample Mendelian randomization (MR) analysis to investigate the relationship between gut microbiota and five main CRDs, including chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), sarcoidosis, and pneumoconiosis. For MR analysis, the inverse variance weighted (IVW) method was utilized as the primary method. The MR-Egger, weighted median, and MR-PRESSO statistical methods were used as a supplement. To detect heterogeneity and pleiotropy, the Cochrane and Rucker Q test, MR-Egger intercept test, and MR-PRESSO global test were then implemented. The leave-one-out strategy was also applied to assess the consistency of the MR results.
RESULTS
Based on substantial genetic data obtained from genome-wide association studies (GWAS) comprising 3,504,473 European participants, our study offers evidence that several gut microbial taxa, including 14 probable microbial taxa (specifically, 5, 3, 2, 3 and 1 for COPD, asthma, IPF, sarcoidosis, and pneumoconiosis, respectively) and 33 possible microbial taxa (specifically, 6, 7, 8, 7 and 5 for COPD, asthma, IPF, sarcoidosis, and pneumoconiosis, respectively) play significant roles in the formation of CRDs.
DISCUSSION
This work implies causal relationships between the gut microbiota and CRDs, thereby shedding new light on the gut microbiota-mediated prevention of CRDs.
PubMed: 37333634
DOI: 10.3389/fmicb.2023.1200937 -
CMAJ : Canadian Medical Association... Feb 2024
Topics: Humans; Middle Aged; Berylliosis; Metal Workers
PubMed: 38346777
DOI: 10.1503/cmaj.221680-f -
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 -
Neurology India Jan 2024
Topics: Humans; Siderosis
PubMed: 38443043
DOI: 10.4103/neurol-india.Neurol-India-D-24-00018