Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis
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....
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Elsevier
2023-12-01
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Series: | Ecotoxicology and Environmental Safety |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323011971 |
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author | Fuyang Jiang Qiyue Jiang Lin Hou Jing Zhao Zhonghui Zhu Qiyue Jia Wenming Xue Hongwei Wang Yan Wang Lin Tian |
author_facet | Fuyang Jiang Qiyue Jiang Lin Hou Jing Zhao Zhonghui Zhu Qiyue Jia Wenming Xue Hongwei Wang Yan Wang Lin Tian |
author_sort | Fuyang Jiang |
collection | DOAJ |
description | 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. |
first_indexed | 2024-03-09T10:53:50Z |
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id | doaj.art-e7f75a1dae1f47eb8d74e0136f742699 |
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issn | 0147-6513 |
language | English |
last_indexed | 2024-03-09T10:53:50Z |
publishDate | 2023-12-01 |
publisher | Elsevier |
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series | Ecotoxicology and Environmental Safety |
spelling | doaj.art-e7f75a1dae1f47eb8d74e0136f7426992023-12-01T05:00:27ZengElsevierEcotoxicology and Environmental Safety0147-65132023-12-01268115693Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosisFuyang Jiang0Qiyue Jiang1Lin Hou2Jing Zhao3Zhonghui Zhu4Qiyue Jia5Wenming Xue6Hongwei Wang7Yan Wang8Lin Tian9Department of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China; Corresponding authors at: Department of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China.Department of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China; Corresponding authors at: Department of Occupational and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China.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.http://www.sciencedirect.com/science/article/pii/S0147651323011971SilicaPulmonary fibrosisPyroptosisGasdermin DMacrophage |
spellingShingle | Fuyang Jiang Qiyue Jiang Lin Hou Jing Zhao Zhonghui Zhu Qiyue Jia Wenming Xue Hongwei Wang Yan Wang Lin Tian Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis Ecotoxicology and Environmental Safety Silica Pulmonary fibrosis Pyroptosis Gasdermin D Macrophage |
title | Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis |
title_full | Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis |
title_fullStr | Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis |
title_full_unstemmed | Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis |
title_short | Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis |
title_sort | inhibition of macrophage pyroptosis ameliorates silica induced pulmonary fibrosis |
topic | Silica Pulmonary fibrosis Pyroptosis Gasdermin D Macrophage |
url | http://www.sciencedirect.com/science/article/pii/S0147651323011971 |
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