Stimulation of rat alveolar macrophage fibronectin release in a cadmium chloride model of lung injury and fibrosis
Rats were exposed to saline or cadmium chloride (CdCl 2) at 25, 100, or 400 μg/kg body weight by intratracheal instillation. At 3, 7, 14, and 28 days after exposure five animals/treatment were euthanized, the lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydr...
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Veröffentlicht in: | Toxicology and applied pharmacology 1992-09, Vol.116 (1), p.30-37 |
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creator | Driscoll, Kevin E. Maurer, James K. Poynter, James Higgins, Janet Asquith, Thomas Miller, Nita Sue |
description | Rats were exposed to saline or cadmium chloride (CdCl
2) at 25, 100, or 400 μg/kg body weight by intratracheal instillation. At 3, 7, 14, and 28 days after exposure five animals/treatment were euthanized, the lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydrogenase (LDH), total protein,
N-acetylglucosamindase (NAG), and cell number, type, and viability. Lung hydroxyproline concentration was characterized as a marker of lung collagen. Alveolar macrophages (AM) obtained in BALF were cultured and the release of fibronectin and TNF was determined. Lung tissue was examined microscopically at 28 and 90 days after exposure. Exposure to CdCl
2 resulted in lung injury and inflammation demonstrated by increases in BALF LDH, total protein, NAG, and inflammatory cells. AM TNF release was not significantly changed by CdCl
2 treatment. All doses of CdCl
2 stimulated AM fibronectin secretion, a response which persisted throughout the 28-day postexposure period examined. Pulmonary fibrosis was demonstrated biochemically and/or histologically (trichrome staining tissue) at all CdCl
2 dose levels. The association of CdCl
2-induced AM fibronectin release with lung fibrosis confirms and extends previous observations relating AM-derived fibronectin to the development of interstitial lung disease and provides further evidence that the persistent increase in AM fibronectin release represents an early indicator of fibrosis. |
doi_str_mv | 10.1016/0041-008X(92)90141-E |
format | Article |
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2) at 25, 100, or 400 μg/kg body weight by intratracheal instillation. At 3, 7, 14, and 28 days after exposure five animals/treatment were euthanized, the lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydrogenase (LDH), total protein,
N-acetylglucosamindase (NAG), and cell number, type, and viability. Lung hydroxyproline concentration was characterized as a marker of lung collagen. Alveolar macrophages (AM) obtained in BALF were cultured and the release of fibronectin and TNF was determined. Lung tissue was examined microscopically at 28 and 90 days after exposure. Exposure to CdCl
2 resulted in lung injury and inflammation demonstrated by increases in BALF LDH, total protein, NAG, and inflammatory cells. AM TNF release was not significantly changed by CdCl
2 treatment. All doses of CdCl
2 stimulated AM fibronectin secretion, a response which persisted throughout the 28-day postexposure period examined. Pulmonary fibrosis was demonstrated biochemically and/or histologically (trichrome staining tissue) at all CdCl
2 dose levels. The association of CdCl
2-induced AM fibronectin release with lung fibrosis confirms and extends previous observations relating AM-derived fibronectin to the development of interstitial lung disease and provides further evidence that the persistent increase in AM fibronectin release represents an early indicator of fibrosis.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/0041-008X(92)90141-E</identifier><identifier>PMID: 1529450</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Bronchoalveolar Lavage Fluid - cytology ; Cadmium - administration & dosage ; Cadmium - toxicity ; Cadmium Chloride ; Cell Count - drug effects ; Chlorides - administration & dosage ; Chlorides - toxicity ; Disease Models, Animal ; Fibronectins - metabolism ; Hydroxyproline - analysis ; Lung - chemistry ; Lung - drug effects ; Lung - pathology ; Macrophages, Alveolar - drug effects ; Macrophages, Alveolar - metabolism ; Male ; Medical sciences ; Pneumology ; Pulmonary Fibrosis - chemically induced ; Rats ; Rats, Inbred F344 ; Respiratory system : syndromes and miscellaneous diseases ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Toxicology and applied pharmacology, 1992-09, Vol.116 (1), p.30-37</ispartof><rights>1992</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-6ab0836b6363e400e1ddc4d43b24aaf2b141186de7b47f27d18344dca910f18f3</citedby><cites>FETCH-LOGICAL-c483t-6ab0836b6363e400e1ddc4d43b24aaf2b141186de7b47f27d18344dca910f18f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0041-008X(92)90141-E$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5573485$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1529450$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Driscoll, Kevin E.</creatorcontrib><creatorcontrib>Maurer, James K.</creatorcontrib><creatorcontrib>Poynter, James</creatorcontrib><creatorcontrib>Higgins, Janet</creatorcontrib><creatorcontrib>Asquith, Thomas</creatorcontrib><creatorcontrib>Miller, Nita Sue</creatorcontrib><title>Stimulation of rat alveolar macrophage fibronectin release in a cadmium chloride model of lung injury and fibrosis</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Rats were exposed to saline or cadmium chloride (CdCl
2) at 25, 100, or 400 μg/kg body weight by intratracheal instillation. At 3, 7, 14, and 28 days after exposure five animals/treatment were euthanized, the lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydrogenase (LDH), total protein,
N-acetylglucosamindase (NAG), and cell number, type, and viability. Lung hydroxyproline concentration was characterized as a marker of lung collagen. Alveolar macrophages (AM) obtained in BALF were cultured and the release of fibronectin and TNF was determined. Lung tissue was examined microscopically at 28 and 90 days after exposure. Exposure to CdCl
2 resulted in lung injury and inflammation demonstrated by increases in BALF LDH, total protein, NAG, and inflammatory cells. AM TNF release was not significantly changed by CdCl
2 treatment. All doses of CdCl
2 stimulated AM fibronectin secretion, a response which persisted throughout the 28-day postexposure period examined. Pulmonary fibrosis was demonstrated biochemically and/or histologically (trichrome staining tissue) at all CdCl
2 dose levels. The association of CdCl
2-induced AM fibronectin release with lung fibrosis confirms and extends previous observations relating AM-derived fibronectin to the development of interstitial lung disease and provides further evidence that the persistent increase in AM fibronectin release represents an early indicator of fibrosis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>Cadmium - administration & dosage</subject><subject>Cadmium - toxicity</subject><subject>Cadmium Chloride</subject><subject>Cell Count - drug effects</subject><subject>Chlorides - administration & dosage</subject><subject>Chlorides - toxicity</subject><subject>Disease Models, Animal</subject><subject>Fibronectins - metabolism</subject><subject>Hydroxyproline - analysis</subject><subject>Lung - chemistry</subject><subject>Lung - drug effects</subject><subject>Lung - pathology</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pneumology</subject><subject>Pulmonary Fibrosis - chemically induced</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFrFTEQx4Mo9Vn9Bgo5iOhh62ST3bd7KUh5WqHQgwrewmwyaVOym2eyW-i3N8991FtPk2F-8yfzY-ytgDMBov0MoEQF0P3-2NefehCl2z1jGwF9W4GU8jnbPCIv2auc7wCgV0qcsBPR1L1qYMPSj9mPS8DZx4lHxxPOHMM9xYCJj2hS3N_iDXHnhxQnMrOfeKJAmImXJ3KDdvTLyM1tiMlb4mO0FA5RYZluCnO3pAeOk10jss-v2QuHIdObYz1lv77ufl5cVlfX375ffLmqjOrkXLU4QCfboZWtJAVAwlqjrJJDrRBdPZSDRdda2g5q6-qtFZ1UyhrsBTjROXnKPqy5-xT_LJRnPfpsKAScKC5Zi1YVC6IvoFrBcm3OiZzeJz9ietAC9EG1PnjUB4-6r_U_1XpX1t4d85dhJPt_aXVb5u-Pc8wGg0s4GZ8fsabZStU1BTtfMSou7j0lnY2nyZD1qfjWNvqn__EXOgKb5Q</recordid><startdate>19920901</startdate><enddate>19920901</enddate><creator>Driscoll, Kevin E.</creator><creator>Maurer, James K.</creator><creator>Poynter, James</creator><creator>Higgins, Janet</creator><creator>Asquith, Thomas</creator><creator>Miller, Nita Sue</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>19920901</creationdate><title>Stimulation of rat alveolar macrophage fibronectin release in a cadmium chloride model of lung injury and fibrosis</title><author>Driscoll, Kevin E. ; Maurer, James K. ; Poynter, James ; Higgins, Janet ; Asquith, Thomas ; Miller, Nita Sue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-6ab0836b6363e400e1ddc4d43b24aaf2b141186de7b47f27d18344dca910f18f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>Cadmium - administration & dosage</topic><topic>Cadmium - toxicity</topic><topic>Cadmium Chloride</topic><topic>Cell Count - drug effects</topic><topic>Chlorides - administration & dosage</topic><topic>Chlorides - toxicity</topic><topic>Disease Models, Animal</topic><topic>Fibronectins - metabolism</topic><topic>Hydroxyproline - analysis</topic><topic>Lung - chemistry</topic><topic>Lung - drug effects</topic><topic>Lung - pathology</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pneumology</topic><topic>Pulmonary Fibrosis - chemically induced</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Driscoll, Kevin E.</creatorcontrib><creatorcontrib>Maurer, James K.</creatorcontrib><creatorcontrib>Poynter, James</creatorcontrib><creatorcontrib>Higgins, Janet</creatorcontrib><creatorcontrib>Asquith, Thomas</creatorcontrib><creatorcontrib>Miller, Nita Sue</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Driscoll, Kevin E.</au><au>Maurer, James K.</au><au>Poynter, James</au><au>Higgins, Janet</au><au>Asquith, Thomas</au><au>Miller, Nita Sue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stimulation of rat alveolar macrophage fibronectin release in a cadmium chloride model of lung injury and fibrosis</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>1992-09-01</date><risdate>1992</risdate><volume>116</volume><issue>1</issue><spage>30</spage><epage>37</epage><pages>30-37</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Rats were exposed to saline or cadmium chloride (CdCl
2) at 25, 100, or 400 μg/kg body weight by intratracheal instillation. At 3, 7, 14, and 28 days after exposure five animals/treatment were euthanized, the lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydrogenase (LDH), total protein,
N-acetylglucosamindase (NAG), and cell number, type, and viability. Lung hydroxyproline concentration was characterized as a marker of lung collagen. Alveolar macrophages (AM) obtained in BALF were cultured and the release of fibronectin and TNF was determined. Lung tissue was examined microscopically at 28 and 90 days after exposure. Exposure to CdCl
2 resulted in lung injury and inflammation demonstrated by increases in BALF LDH, total protein, NAG, and inflammatory cells. AM TNF release was not significantly changed by CdCl
2 treatment. All doses of CdCl
2 stimulated AM fibronectin secretion, a response which persisted throughout the 28-day postexposure period examined. Pulmonary fibrosis was demonstrated biochemically and/or histologically (trichrome staining tissue) at all CdCl
2 dose levels. The association of CdCl
2-induced AM fibronectin release with lung fibrosis confirms and extends previous observations relating AM-derived fibronectin to the development of interstitial lung disease and provides further evidence that the persistent increase in AM fibronectin release represents an early indicator of fibrosis.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>1529450</pmid><doi>10.1016/0041-008X(92)90141-E</doi><tpages>8</tpages></addata></record> |
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source | MEDLINE; Access via ScienceDirect (Elsevier) |
subjects | Animals Biological and medical sciences Bronchoalveolar Lavage Fluid - cytology Cadmium - administration & dosage Cadmium - toxicity Cadmium Chloride Cell Count - drug effects Chlorides - administration & dosage Chlorides - toxicity Disease Models, Animal Fibronectins - metabolism Hydroxyproline - analysis Lung - chemistry Lung - drug effects Lung - pathology Macrophages, Alveolar - drug effects Macrophages, Alveolar - metabolism Male Medical sciences Pneumology Pulmonary Fibrosis - chemically induced Rats Rats, Inbred F344 Respiratory system : syndromes and miscellaneous diseases Tumor Necrosis Factor-alpha - metabolism |
title | Stimulation of rat alveolar macrophage fibronectin release in a cadmium chloride model of lung injury and fibrosis |
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