Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis
We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2002-07, Vol.27 (1), p.78-84 |
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| container_title | American journal of respiratory cell and molecular biology |
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| creator | Borges, Valeria M Lopes, Marcela F Falcao, Haroldo Leite-Junior, Jose Henrique Rocco, Patricia R. M Davidson, Wendy F Linden, Rafael Zin, Walter A DosReis, George A |
| description | We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host. |
| doi_str_mv | 10.1165/ajrcmb.27.1.4717 |
| format | Article |
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M ; Davidson, Wendy F ; Linden, Rafael ; Zin, Walter A ; DosReis, George A</creator><creatorcontrib>Borges, Valeria M ; Lopes, Marcela F ; Falcao, Haroldo ; Leite-Junior, Jose Henrique ; Rocco, Patricia R. M ; Davidson, Wendy F ; Linden, Rafael ; Zin, Walter A ; DosReis, George A</creatorcontrib><description>We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/ajrcmb.27.1.4717</identifier><identifier>PMID: 12091249</identifier><identifier>CODEN: AJRBEL</identifier><language>eng</language><publisher>United States: Am Thoracic Soc</publisher><subject>Acute Disease ; Animals ; Animals, Genetically Modified ; Apoptosis - immunology ; Apoptosis - physiology ; Caspase Inhibitors ; Cell Division - drug effects ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Fas Ligand Protein ; Lymph Nodes - drug effects ; Lymph Nodes - immunology ; Lymph Nodes - pathology ; Lymphocytes - immunology ; Macrophages - immunology ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Inbred BALB C ; Neutrophils - drug effects ; Silicon Dioxide - adverse effects ; Silicosis - etiology ; Silicosis - immunology ; Silicosis - pathology ; Thorax - immunology ; Thorax - physiology</subject><ispartof>American journal of respiratory cell and molecular biology, 2002-07, Vol.27 (1), p.78-84</ispartof><rights>Copyright American Lung Association Jul 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-cc1cf00e9bba5a5f86bd7e4a0192f5de43854b69a12da19548448552d0aabd3e3</citedby><cites>FETCH-LOGICAL-c354t-cc1cf00e9bba5a5f86bd7e4a0192f5de43854b69a12da19548448552d0aabd3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12091249$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Borges, Valeria M</creatorcontrib><creatorcontrib>Lopes, Marcela F</creatorcontrib><creatorcontrib>Falcao, Haroldo</creatorcontrib><creatorcontrib>Leite-Junior, Jose Henrique</creatorcontrib><creatorcontrib>Rocco, Patricia R. M</creatorcontrib><creatorcontrib>Davidson, Wendy F</creatorcontrib><creatorcontrib>Linden, Rafael</creatorcontrib><creatorcontrib>Zin, Walter A</creatorcontrib><creatorcontrib>DosReis, George A</creatorcontrib><title>Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Apoptosis - immunology</subject><subject>Apoptosis - physiology</subject><subject>Caspase Inhibitors</subject><subject>Cell Division - drug effects</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fas Ligand Protein</subject><subject>Lymph Nodes - drug effects</subject><subject>Lymph Nodes - immunology</subject><subject>Lymph Nodes - pathology</subject><subject>Lymphocytes - immunology</subject><subject>Macrophages - immunology</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neutrophils - drug effects</subject><subject>Silicon Dioxide - adverse effects</subject><subject>Silicosis - etiology</subject><subject>Silicosis - immunology</subject><subject>Silicosis - pathology</subject><subject>Thorax - immunology</subject><subject>Thorax - physiology</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpFkDtPwzAURi0EolDYmVDEwpTi61wn8VgqHpWKGKCz5ThO4yov7ESIf09KIzH5Duc7lg4hN0AXADF_UHun62zBkgUsMIHkhFwAj3iIIhWn400RQ-AoZuTS-z2lwFKAczIDRgUwFBfkcdm1Xd9664NtkxtXWeODdV0PTdupvmx3prE6eDO6VI31tQ9sEyz10Jvgw1ZWH4ZX5KxQlTfX0zsn2-enz9VruHl_Wa-Wm1BHHPtQa9AFpUZkmeKKF2mc5YlBRUGwgucGo5RjFgsFLFcgOKaIKecsp0pleWSiObk7ejvXfg3G93LfDq4Zv5SMJjFSZDhC9Ahp13rvTCE7Z2vlfiRQeWgmj80kSyTIQ7Nxcjt5h6w2-f9gijQC90egtLvy2zojfa2qasRhsv3JkjT6BcB7dx0</recordid><startdate>20020701</startdate><enddate>20020701</enddate><creator>Borges, Valeria M</creator><creator>Lopes, Marcela F</creator><creator>Falcao, Haroldo</creator><creator>Leite-Junior, Jose Henrique</creator><creator>Rocco, Patricia R. 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Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.</abstract><cop>United States</cop><pub>Am Thoracic Soc</pub><pmid>12091249</pmid><doi>10.1165/ajrcmb.27.1.4717</doi><tpages>7</tpages></addata></record> |
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| subjects | Acute Disease Animals Animals, Genetically Modified Apoptosis - immunology Apoptosis - physiology Caspase Inhibitors Cell Division - drug effects Disease Models, Animal Enzyme Inhibitors - pharmacology Fas Ligand Protein Lymph Nodes - drug effects Lymph Nodes - immunology Lymph Nodes - pathology Lymphocytes - immunology Macrophages - immunology Membrane Glycoproteins - metabolism Mice Mice, Inbred BALB C Neutrophils - drug effects Silicon Dioxide - adverse effects Silicosis - etiology Silicosis - immunology Silicosis - pathology Thorax - immunology Thorax - physiology |
| title | Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis |
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