Background: The aim was to explore the effect of macrophage polarization and macrophage-to-myofibroblast transition (MMT) in silicosis.
Methods: Male Wistar rats were divided into a control group and a silicosis group developed using a HOPE MED 8050 dynamic automatic dusting system. Murine macrophage MH-S cells were randomly divided into a control group and an SiO group. The pathological changes in lung tissue were observed using hematoxylin and eosin (HE) and Van Gieson (VG) staining. The distribution and location of macrophage marker (F4/80), M1 macrophage marker (iNOS), M2 macrophage marker (CD206), and myofibroblast marker (α-smooth muscle actin [α-SMA]) were detected using immunohistochemical and immunofluorescent staining. The expression changes in iNOS, Arg, α-SMA, vimentin, and type I collagen (Col I) were measured using Western blot.
Results: The results of HE and VG staining showed obvious silicon nodule formation and the distribution of thick collagen fibers in the lung tissue of the silicosis group. Macrophage marker F4/80 increased gradually from 8 to 32 weeks after exposure to silica. Immunohistochemical and immunofluorescent staining results revealed that there were more iNOS-positive cells and some CD206-positive cells in the lung tissue of the silicosis group at 8 weeks. More CD206-positive cells were found in the silicon nodules of the lung tissues in the silicosis group at 32 weeks. Western blot analysis showed that the expressions of Inducible nitric oxide synthase and Arg protein in the lung tissues of the silicosis group were upregulated compared with those of the control group. The results of immunofluorescence staining showed the co-expression of F4/80, α-SMA, and Col I, and CD206 and α-SMA were co-expressed in the lung tissue of the silicosis group. The extracted rat alveolar lavage fluid revealed F4/80α-SMA, CD206α-SMA, and F4/80α-SMACol I cells using immunofluorescence staining. Similar results were also found in MH-S cells induced by SiO.
Conclusions: The development of silicosis is accompanied by macrophage polarization and MMT.
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http://dx.doi.org/10.1002/ame2.12470 | DOI Listing |
Toxicology
December 2024
Molecular Toxicology Laboratory of Sichuan Provincial Education office, Institute of Systems Epidemiology, West China School of Public Health and West China Fourth Hospital, Sichuan University Chengdu, 610041, China; West China Occupational Pneumoconiosis Cohort Study (WCOPCS) working group, Research Center for Prevention and Therapy of Occupational Disease, West China-PUMC C.C. Chen Institute of Health, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China. Electronic address:
Apoptosis of alveolar macrophages (AMs) induced by silica is one of the crucial driving factors of silicosis inflammation and fibrosis. However, the mechanism of silica-induced AMs apoptosis remains unclear. In this study, transcriptome sequencing identified 11 differentially expressed (DE)-mRNAs enriched in the regulation of apoptotic signaling pathways in AMs treated with 250 μg/mL silica for 24 h, of which tripartite motif-containing 32 (Trim32) was the most significant and down-regulated.
View Article and Find Full Text PDFIn Vivo
December 2024
College of Biology, Hunan University, Changsha, P.R. China;
Background/aim: Silicosis, the most severe type of occupational pneumoconiosis, leads to diffuse pulmonary fibrosis without specific therapy. Ferroptosis is triggered by reactive oxygen species (ROS) and Fe overload-induced lipid peroxidation, which is involved in the progression of pulmonary fibrosis. As an important coenzyme in the process of aerobic respiration, Coenzyme Q10 (CoQ10) can enhance mitochondrial function and energy supply and reduce malondialdehyde (MDA) to limit the risk of fibrosis.
View Article and Find Full Text PDFOccup Environ Med
December 2024
School of Public Health, Division of Environmental and Occupational Health Sciences, University of Illinois Chicago, Chicago, Illinois, USA.
Introduction: Previous studies suggest respirable crystalline silica (RCS) is an important driver of resurgent pneumoconiosis among US coal miners. Although greater attention has been focused on dust exposures in underground coal miners, surface miners are also at risk of severe disease. This study explores RCS exposure in this population.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
School of Public Health, Xinxiang Medical University, Xinxiang 453003, China; School of Public Health, North China University of Science and Technology, Tangshan 063000, China. Electronic address:
Silicosis is a life-threatening occupational disease because of inhaling silica dust, leading to chronic inflammation, pyroptosis, and fibrosis. Unfortunately, it is still lacking effective pharmacological intervention currently. Honokiol (HKL), a natural extract with biological activity from Magnolia bark, is known for its antioxidant and anti-inflammatory biological effects.
View Article and Find Full Text PDFEcotoxicol Environ Saf
December 2024
NHC Key Laboratory of Pneumoconiosis, Shanxi Province Key Laboratory of Respiratory, Department of Respiratory and Critical Care Medicine, Shanxi Medical University Affiliated First Hospital, Taiyuan 030000, China. Electronic address:
Silicosis is a systemic disease marked by diffuse pulmonary fibrosis resulting from prolonged inhalation of crystalline silica (CS) dust. This study aimed to examine the effects of anisodamine (ANI) on pulmonary inflammation and fibrosis in silicosis, as well as to elucidate the underlying molecular mechanisms. Animal experiments demonstrated that ANI significantly reduced alveolar structure damage and the formation of silicosis nodules in affected mice, as confirmed by pathological slides.
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