NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis
Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contributi...
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| Published in: | Respiratory research Vol. 26; no. 1; pp. 109 - 17 |
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| Main Authors: | , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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BioMed Central
21.03.2025
BioMed Central Ltd Nature Publishing Group BMC |
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| ISSN: | 1465-993X, 1465-9921, 1465-993X |
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| Abstract | Background
Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease.
Methods
The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung.
Results
Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F
−
and fibrotic Siglec-F
+
neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity.
Conclusions
These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. |
|---|---|
| AbstractList | Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease. The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung. Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1[beta] and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F.sup.- and fibrotic Siglec-F.sup.+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity. These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGF[beta]-mediated myofibroblast activation, tissue damage, and fibrosis. Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease. The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung. Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F and fibrotic Siglec-F neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity. These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. BackgroundSilicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease.MethodsThe in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung.ResultsIntranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F− and fibrotic Siglec-F+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity.ConclusionsThese findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. Abstract Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease. Methods The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung. Results Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F− and fibrotic Siglec-F+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity. Conclusions These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease. Methods The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung. Results Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F − and fibrotic Siglec-F + neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity. Conclusions These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease.BACKGROUNDSilicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease.The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung.METHODSThe in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung.Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F- and fibrotic Siglec-F+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity.RESULTSIntranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1β and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F- and fibrotic Siglec-F+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity.These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis.CONCLUSIONSThese findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGFβ-mediated myofibroblast activation, tissue damage, and fibrosis. Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica. Accumulating evidence has implicated a role for NLRP3 in silicosis pathogenesis. In this study, we mechanistically elucidated the contribution of NLRP3 to silica-induced pulmonary disease. Methods The in vivo role of NLRP3 was investigated following intranasal delivery of 2 mg of silica or diluent alone to wildtype, NLRP3 reporter, and NLRP3-deficient mice. Protein expression, inflammation, and histopathology were analyzed in the lung. Results Intranasal administration of silica recapitulated the key pathological features of human silicosis, including nonresolving inflammation, the formation of silicotic nodules, and diffuse lung fibrosis. A reporter mouse placed under the native NLRP3 promoter revealed silica rapidly upregulated NLRP3 expression throughout the lung. NLRP3-deficient mice displayed marked early reductions in silica-induced IL-1[beta] and IL-18 levels in the airways. Additionally, NLRP3 deficiency impaired the rapid infiltration of conventional Siglec-F.sup.- and fibrotic Siglec-F.sup.+ neutrophils, which correlated with reduced levels of neutrophil elastase. Deficiency in acute NLRP3-mediated inflammation correlated with significantly reduced pulmonary transforming growth factor beta and alpha smooth muscle actin expression, tissue damage, and fibrosis in the chronic phase of disease progression. Importantly, this included reduced silicotic nodule size and cellularity. Conclusions These findings highlight a major detrimental role for the NLRP3 inflammasome in driving silica-induced pulmonary neutrophil infiltration, TGF[beta]-mediated myofibroblast activation, tissue damage, and fibrosis. Keywords: Silicosis, NLRP3 inflammasome, Mouse model, Inflammation, Fibrosis |
| ArticleNumber | 109 |
| Audience | Academic |
| Author | Barry, Kristian T. Ong, James D. H. Rosli, Sarah Dousha, Lovisa Tate, Michelle D. West, Alison C. Harpur, Christopher M. Hertzog, Paul J. Mansell, Ashley Hodges, Christopher J. Lam, Maggie |
| Author_xml | – sequence: 1 givenname: Maggie surname: Lam fullname: Lam, Maggie organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 2 givenname: Kristian T. surname: Barry fullname: Barry, Kristian T. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 3 givenname: Christopher J. surname: Hodges fullname: Hodges, Christopher J. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 4 givenname: Christopher M. surname: Harpur fullname: Harpur, Christopher M. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 5 givenname: James D. H. surname: Ong fullname: Ong, James D. H. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 6 givenname: Sarah surname: Rosli fullname: Rosli, Sarah organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 7 givenname: Alison C. surname: West fullname: West, Alison C. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 8 givenname: Lovisa surname: Dousha fullname: Dousha, Lovisa organization: Monash Lung, Sleep, Allergy, and Immunology, Monash Medical Centre, Department of Medicine, Monash University – sequence: 9 givenname: Paul J. surname: Hertzog fullname: Hertzog, Paul J. organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University – sequence: 10 givenname: Ashley surname: Mansell fullname: Mansell, Ashley organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University, Department of Microbiology, Anatomy, Physiology, and Pharmacology, La Trobe University – sequence: 11 givenname: Michelle D. surname: Tate fullname: Tate, Michelle D. email: michelle.tate@hudson.org.au organization: Centre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Department of Molecular Translational Sciences, Monash University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40119408$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1038/ni.1631 10.1186/1743-8977-10-3 10.3389/fphar.2024.1362509 10.1111/jcmm.12341 10.3390/cells13171508 10.1111/imr.13406 10.1016/j.jaci.2021.09.031 10.1189/jlb.3HI1014-493R 10.1038/s41419-023-06258-1 10.1016/j.cell.2010.01.040 10.1016/S2213-2600(24)00007-9 10.1111/imcb.12459 10.1038/s41598-019-50725-9 10.1097/MCP.0000000000001020 10.1016/j.bbrc.2020.03.122 10.1189/jlb.4MR0616-288R 10.1183/23120541.00883-2020 10.3390/v12040401 10.1111/bph.14787 10.1038/s41577-019-0215-7 10.1016/j.toxlet.2021.09.014 10.1016/j.biopha.2019.108756 10.3109/08977194.2011.595714 10.1148/126.2.359 10.1371/journal.pgen.1010515 10.1002/ajim.23561 10.4049/jimmunol.0901363 10.3389/fimmu.2020.613170 10.1186/s12989-014-0058-0 10.1165/rcmb.2021-0545TR 10.3892/ijmm.2024.5349 10.1186/s12989-024-00611-8 10.1080/15459624.2020.1798011 10.1038/s41467-018-07425-1 10.1111/imr.12884 10.1016/S0076-6879(10)77013-0 10.1073/pnas.2008006117 10.1126/science.abi5934 10.1007/978-1-0716-3331-1_9 10.1002/eji.201747404 10.1016/S1074-7613(04)00055-X 10.1073/pnas.0803933105 10.1016/j.disamonth.2007.09.020 10.1016/j.ecoenv.2023.115693 10.1016/j.bbrc.2018.11.129 10.1172/JCI156876 10.1093/infdis/jiad566 10.1038/cr.2015.139 10.1016/j.celrep.2020.108164 10.1159/000334247 10.1378/chest.55.4.274 10.1073/pnas.0605669103 10.1186/s12989-014-0069-x 10.1002/cti2.1455 10.1016/B978-0-12-386456-7.05308-9 10.1007/s10495-021-01663-3 10.1016/j.ecoenv.2020.110364 10.1186/s12989-021-00434-x 10.1136/oem.2003.009357 10.1111/resp.14242 10.1038/s41401-021-00693-6 10.1016/1043-4666(93)90024-Y 10.1016/j.matbio.2018.02.004 10.4049/jimmunol.1201447 10.1038/s41598-020-73056-6 |
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| Keywords | Mouse model Inflammation NLRP3 inflammasome Silicosis Fibrosis |
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| References_xml | – ident: 3192_CR14 doi: 10.1038/ni.1631 – ident: 3192_CR46 doi: 10.1186/1743-8977-10-3 – ident: 3192_CR61 doi: 10.3389/fphar.2024.1362509 – ident: 3192_CR38 doi: 10.1111/jcmm.12341 – ident: 3192_CR28 doi: 10.3390/cells13171508 – ident: 3192_CR51 doi: 10.1111/imr.13406 – ident: 3192_CR60 doi: 10.1016/j.jaci.2021.09.031 – ident: 3192_CR37 doi: 10.1189/jlb.3HI1014-493R – ident: 3192_CR32 doi: 10.1038/s41419-023-06258-1 – ident: 3192_CR43 doi: 10.1016/j.cell.2010.01.040 – ident: 3192_CR5 doi: 10.1016/S2213-2600(24)00007-9 – ident: 3192_CR57 doi: 10.1111/imcb.12459 – ident: 3192_CR34 doi: 10.1038/s41598-019-50725-9 – ident: 3192_CR7 doi: 10.1097/MCP.0000000000001020 – ident: 3192_CR59 doi: 10.1016/j.bbrc.2020.03.122 – ident: 3192_CR17 doi: 10.1189/jlb.4MR0616-288R – ident: 3192_CR31 doi: 10.1183/23120541.00883-2020 – ident: 3192_CR39 doi: 10.3390/v12040401 – ident: 3192_CR56 doi: 10.1111/bph.14787 – ident: 3192_CR21 doi: 10.1038/s41577-019-0215-7 – ident: 3192_CR25 doi: 10.1016/j.toxlet.2021.09.014 – ident: 3192_CR64 doi: 10.1016/j.biopha.2019.108756 – ident: 3192_CR62 doi: 10.3109/08977194.2011.595714 – ident: 3192_CR9 doi: 10.1148/126.2.359 – ident: 3192_CR35 doi: 10.1371/journal.pgen.1010515 – ident: 3192_CR12 doi: 10.1002/ajim.23561 – ident: 3192_CR49 doi: 10.4049/jimmunol.0901363 – ident: 3192_CR54 doi: 10.3389/fimmu.2020.613170 – ident: 3192_CR44 doi: 10.1186/s12989-014-0058-0 – ident: 3192_CR1 doi: 10.1165/rcmb.2021-0545TR – ident: 3192_CR47 doi: 10.3892/ijmm.2024.5349 – ident: 3192_CR16 doi: 10.1186/s12989-024-00611-8 – ident: 3192_CR4 doi: 10.1080/15459624.2020.1798011 – ident: 3192_CR50 doi: 10.1038/s41467-018-07425-1 – ident: 3192_CR52 doi: 10.1111/imr.12884 – ident: 3192_CR29 doi: 10.1016/S0076-6879(10)77013-0 – ident: 3192_CR15 doi: 10.1073/pnas.2008006117 – ident: 3192_CR18 doi: 10.1126/science.abi5934 – ident: 3192_CR30 doi: 10.1007/978-1-0716-3331-1_9 – ident: 3192_CR19 doi: 10.1002/eji.201747404 – ident: 3192_CR42 doi: 10.1016/S1074-7613(04)00055-X – ident: 3192_CR27 doi: 10.1073/pnas.0803933105 – ident: 3192_CR23 doi: 10.1016/j.disamonth.2007.09.020 – ident: 3192_CR45 doi: 10.1016/j.ecoenv.2023.115693 – ident: 3192_CR63 doi: 10.1016/j.bbrc.2018.11.129 – ident: 3192_CR36 doi: 10.1172/JCI156876 – ident: 3192_CR33 doi: 10.1093/infdis/jiad566 – ident: 3192_CR20 doi: 10.1038/cr.2015.139 – ident: 3192_CR58 doi: 10.1016/j.celrep.2020.108164 – ident: 3192_CR13 doi: 10.1159/000334247 – ident: 3192_CR8 doi: 10.1378/chest.55.4.274 – ident: 3192_CR40 doi: 10.1073/pnas.0605669103 – ident: 3192_CR65 doi: 10.1186/s12989-014-0069-x – ident: 3192_CR55 doi: 10.1002/cti2.1455 – ident: 3192_CR10 doi: 10.1016/B978-0-12-386456-7.05308-9 – ident: 3192_CR22 doi: 10.1007/s10495-021-01663-3 – ident: 3192_CR24 doi: 10.1016/j.ecoenv.2020.110364 – ident: 3192_CR6 – ident: 3192_CR11 doi: 10.1186/s12989-021-00434-x – ident: 3192_CR3 doi: 10.1136/oem.2003.009357 – ident: 3192_CR2 doi: 10.1111/resp.14242 – ident: 3192_CR48 doi: 10.1038/s41401-021-00693-6 – ident: 3192_CR66 doi: 10.1016/1043-4666(93)90024-Y – ident: 3192_CR41 doi: 10.1016/j.matbio.2018.02.004 – ident: 3192_CR53 doi: 10.4049/jimmunol.1201447 – ident: 3192_CR26 doi: 10.1038/s41598-020-73056-6 |
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Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica.... Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica.... Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica.... BackgroundSilicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated by silica.... Abstract Background Silicosis is a progressive and often fatal occupational lung disease. The NLRP3 inflammasome is an innate immune sensor that is activated... |
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| SubjectTerms | Actin Animals Cell activation Complications and side effects Damage Development and progression Elastase Fibrosis Growth factors Health aspects Histopathology In vivo methods and tests Infiltration Inflammasomes Inflammasomes - metabolism Inflammation Intranasal administration Lasers Leukocytes (neutrophilic) Lung - drug effects Lung - immunology Lung - metabolism Lung - pathology Lung diseases Lung nodules Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Knockout Mouse model Neutrophil Infiltration - drug effects Neutrophil Infiltration - physiology Neutrophils NLR Family, Pyrin Domain-Containing 3 Protein - deficiency NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLRP3 NLRP3 inflammasome Nodules Occupational diseases Pathogenesis Pneumology/Respiratory System Protein expression Proteins Pulmonary fibrosis Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - genetics Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology Pulmonary Fibrosis - prevention & control Silica Silica dust Silicon dioxide Silicon Dioxide - administration & dosage Silicon Dioxide - toxicity Silicosis Silicosis - genetics Silicosis - metabolism Silicosis - pathology Smooth muscle Stem cells |
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| Title | NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis |
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