Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice
Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF)...
Gespeichert in:
| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2005-11, Vol.65 (21), p.9670-9677 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 9677 |
|---|---|
| container_issue | 21 |
| container_start_page | 9670 |
| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 65 |
| creator | HAEGENS, Astrid VAN DER VLIET, Albert MOSSMAN, Brooke T BUTNOR, Kelly J HEINTZ, Nicholas TAATJES, Douglas HEMENWAY, David VACEK, Pamela FREEMAN, Bruce A HAZEN, Stanley L BRENNAN, Marie Luise |
| description | Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPO-/-) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestos-exposed myeloperoxidase-null versus normal mice. Asbestos-associated lung inflammation in myeloperoxidase-null mice was reduced (P < or = 0.05) in comparison with normal asbestos-exposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P < or = 0.05) in Ki-67- and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation. |
| doi_str_mv | 10.1158/0008-5472.CAN-05-1751 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_17387124</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17387124</sourcerecordid><originalsourceid>FETCH-LOGICAL-c515t-a33920f4e1fccceaa69fceec2b7a2449c29e8e0b9b1e5c6da22536c939ed734b3</originalsourceid><addsrcrecordid>eNpFkE1LxDAQhoMoun78BKUXvWVN0qZtjsviF4he9Bym6VQjabomLei_N8WipyHwvJl3HkLOOVtzLutrxlhNZVGJ9XbzRJmkvJJ8j6y4zGtaFYXcJ6s_5ogcx_iRnpIzeUiOeCnKUtXlivSb2GAch0itbyeDbeYm_5ZZ3znoexjt4DPwbYY7O76js-Ayg85luzA422FYiIAZuBFDyluf9d_ohh2G4cu2EJH6KSV6a_CUHHTgIp4t84S83t68bO_p4_Pdw3bzSI3kcqSQ50qwrkDeGWMQoFSdQTSiqUAUhTJCYY2sUQ1HacoWhJB5aVSusK3yoslPyNXvv6nm55Tu072Nc2_wOExR8yqvKy6KBMpf0IQhxoCd3gXbQ_jWnOnZs54d6tmhTp41k3r2nHIXy4Kp6bH9Ty1iE3C5ABANuC6ANzb-c5XgSqYCPzEziTE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17387124</pqid></control><display><type>article</type><title>Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice</title><source>MEDLINE</source><source>American Association for Cancer Research Journals</source><source>EZB Electronic Journals Library</source><creator>HAEGENS, Astrid ; VAN DER VLIET, Albert ; MOSSMAN, Brooke T ; BUTNOR, Kelly J ; HEINTZ, Nicholas ; TAATJES, Douglas ; HEMENWAY, David ; VACEK, Pamela ; FREEMAN, Bruce A ; HAZEN, Stanley L ; BRENNAN, Marie Luise</creator><creatorcontrib>HAEGENS, Astrid ; VAN DER VLIET, Albert ; MOSSMAN, Brooke T ; BUTNOR, Kelly J ; HEINTZ, Nicholas ; TAATJES, Douglas ; HEMENWAY, David ; VACEK, Pamela ; FREEMAN, Bruce A ; HAZEN, Stanley L ; BRENNAN, Marie Luise</creatorcontrib><description>Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPO-/-) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestos-exposed myeloperoxidase-null versus normal mice. Asbestos-associated lung inflammation in myeloperoxidase-null mice was reduced (P < or = 0.05) in comparison with normal asbestos-exposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P < or = 0.05) in Ki-67- and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-05-1751</identifier><identifier>PMID: 16266986</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Asbestos - toxicity ; Biological and medical sciences ; Bronchoalveolar Lavage Fluid ; Carcinogenesis, carcinogens and anticarcinogens ; Cell Growth Processes - drug effects ; Cell Growth Processes - physiology ; Chemical agents ; Chemical and industrial products toxicology. Toxic occupational diseases ; Cyclin D1 - metabolism ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - enzymology ; Inhalation Exposure ; Male ; Medical sciences ; Metals and various inorganic compounds ; Mice ; Mice, Inbred C57BL ; Peroxidase - deficiency ; Peroxidase - metabolism ; Pneumonia - chemically induced ; Pneumonia - enzymology ; Toxicology ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 2005-11, Vol.65 (21), p.9670-9677</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-a33920f4e1fccceaa69fceec2b7a2449c29e8e0b9b1e5c6da22536c939ed734b3</citedby><cites>FETCH-LOGICAL-c515t-a33920f4e1fccceaa69fceec2b7a2449c29e8e0b9b1e5c6da22536c939ed734b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3354,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17219524$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16266986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HAEGENS, Astrid</creatorcontrib><creatorcontrib>VAN DER VLIET, Albert</creatorcontrib><creatorcontrib>MOSSMAN, Brooke T</creatorcontrib><creatorcontrib>BUTNOR, Kelly J</creatorcontrib><creatorcontrib>HEINTZ, Nicholas</creatorcontrib><creatorcontrib>TAATJES, Douglas</creatorcontrib><creatorcontrib>HEMENWAY, David</creatorcontrib><creatorcontrib>VACEK, Pamela</creatorcontrib><creatorcontrib>FREEMAN, Bruce A</creatorcontrib><creatorcontrib>HAZEN, Stanley L</creatorcontrib><creatorcontrib>BRENNAN, Marie Luise</creatorcontrib><title>Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPO-/-) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestos-exposed myeloperoxidase-null versus normal mice. Asbestos-associated lung inflammation in myeloperoxidase-null mice was reduced (P < or = 0.05) in comparison with normal asbestos-exposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P < or = 0.05) in Ki-67- and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation.</description><subject>Animals</subject><subject>Asbestos - toxicity</subject><subject>Biological and medical sciences</subject><subject>Bronchoalveolar Lavage Fluid</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Cell Growth Processes - drug effects</subject><subject>Cell Growth Processes - physiology</subject><subject>Chemical agents</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Cyclin D1 - metabolism</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - enzymology</subject><subject>Inhalation Exposure</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Peroxidase - deficiency</subject><subject>Peroxidase - metabolism</subject><subject>Pneumonia - chemically induced</subject><subject>Pneumonia - enzymology</subject><subject>Toxicology</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LxDAQhoMoun78BKUXvWVN0qZtjsviF4he9Bym6VQjabomLei_N8WipyHwvJl3HkLOOVtzLutrxlhNZVGJ9XbzRJmkvJJ8j6y4zGtaFYXcJ6s_5ogcx_iRnpIzeUiOeCnKUtXlivSb2GAch0itbyeDbeYm_5ZZ3znoexjt4DPwbYY7O76js-Ayg85luzA422FYiIAZuBFDyluf9d_ohh2G4cu2EJH6KSV6a_CUHHTgIp4t84S83t68bO_p4_Pdw3bzSI3kcqSQ50qwrkDeGWMQoFSdQTSiqUAUhTJCYY2sUQ1HacoWhJB5aVSusK3yoslPyNXvv6nm55Tu072Nc2_wOExR8yqvKy6KBMpf0IQhxoCd3gXbQ_jWnOnZs54d6tmhTp41k3r2nHIXy4Kp6bH9Ty1iE3C5ABANuC6ANzb-c5XgSqYCPzEziTE</recordid><startdate>20051101</startdate><enddate>20051101</enddate><creator>HAEGENS, Astrid</creator><creator>VAN DER VLIET, Albert</creator><creator>MOSSMAN, Brooke T</creator><creator>BUTNOR, Kelly J</creator><creator>HEINTZ, Nicholas</creator><creator>TAATJES, Douglas</creator><creator>HEMENWAY, David</creator><creator>VACEK, Pamela</creator><creator>FREEMAN, Bruce A</creator><creator>HAZEN, Stanley L</creator><creator>BRENNAN, Marie Luise</creator><general>American Association for Cancer Research</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>7T5</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20051101</creationdate><title>Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice</title><author>HAEGENS, Astrid ; VAN DER VLIET, Albert ; MOSSMAN, Brooke T ; BUTNOR, Kelly J ; HEINTZ, Nicholas ; TAATJES, Douglas ; HEMENWAY, David ; VACEK, Pamela ; FREEMAN, Bruce A ; HAZEN, Stanley L ; BRENNAN, Marie Luise</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-a33920f4e1fccceaa69fceec2b7a2449c29e8e0b9b1e5c6da22536c939ed734b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Asbestos - toxicity</topic><topic>Biological and medical sciences</topic><topic>Bronchoalveolar Lavage Fluid</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Cell Growth Processes - drug effects</topic><topic>Cell Growth Processes - physiology</topic><topic>Chemical agents</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Cyclin D1 - metabolism</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - enzymology</topic><topic>Inhalation Exposure</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Peroxidase - deficiency</topic><topic>Peroxidase - metabolism</topic><topic>Pneumonia - chemically induced</topic><topic>Pneumonia - enzymology</topic><topic>Toxicology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HAEGENS, Astrid</creatorcontrib><creatorcontrib>VAN DER VLIET, Albert</creatorcontrib><creatorcontrib>MOSSMAN, Brooke T</creatorcontrib><creatorcontrib>BUTNOR, Kelly J</creatorcontrib><creatorcontrib>HEINTZ, Nicholas</creatorcontrib><creatorcontrib>TAATJES, Douglas</creatorcontrib><creatorcontrib>HEMENWAY, David</creatorcontrib><creatorcontrib>VACEK, Pamela</creatorcontrib><creatorcontrib>FREEMAN, Bruce A</creatorcontrib><creatorcontrib>HAZEN, Stanley L</creatorcontrib><creatorcontrib>BRENNAN, Marie Luise</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>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HAEGENS, Astrid</au><au>VAN DER VLIET, Albert</au><au>MOSSMAN, Brooke T</au><au>BUTNOR, Kelly J</au><au>HEINTZ, Nicholas</au><au>TAATJES, Douglas</au><au>HEMENWAY, David</au><au>VACEK, Pamela</au><au>FREEMAN, Bruce A</au><au>HAZEN, Stanley L</au><au>BRENNAN, Marie Luise</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2005-11-01</date><risdate>2005</risdate><volume>65</volume><issue>21</issue><spage>9670</spage><epage>9677</epage><pages>9670-9677</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPO-/-) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestos-exposed myeloperoxidase-null versus normal mice. Asbestos-associated lung inflammation in myeloperoxidase-null mice was reduced (P < or = 0.05) in comparison with normal asbestos-exposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P < or = 0.05) in Ki-67- and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>16266986</pmid><doi>10.1158/0008-5472.CAN-05-1751</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 2005-11, Vol.65 (21), p.9670-9677 |
| issn | 0008-5472 1538-7445 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_17387124 |
| source | MEDLINE; American Association for Cancer Research Journals; EZB Electronic Journals Library |
| subjects | Animals Asbestos - toxicity Biological and medical sciences Bronchoalveolar Lavage Fluid Carcinogenesis, carcinogens and anticarcinogens Cell Growth Processes - drug effects Cell Growth Processes - physiology Chemical agents Chemical and industrial products toxicology. Toxic occupational diseases Cyclin D1 - metabolism Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - enzymology Inhalation Exposure Male Medical sciences Metals and various inorganic compounds Mice Mice, Inbred C57BL Peroxidase - deficiency Peroxidase - metabolism Pneumonia - chemically induced Pneumonia - enzymology Toxicology Tumors |
| title | Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T17%3A35%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Asbestos-induced%20lung%20inflammation%20and%20epithelial%20cell%20proliferation%20are%20altered%20in%20myeloperoxidase-null%20mice&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=HAEGENS,%20Astrid&rft.date=2005-11-01&rft.volume=65&rft.issue=21&rft.spage=9670&rft.epage=9677&rft.pages=9670-9677&rft.issn=0008-5472&rft.eissn=1538-7445&rft.coden=CNREA8&rft_id=info:doi/10.1158/0008-5472.CAN-05-1751&rft_dat=%3Cproquest_cross%3E17387124%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17387124&rft_id=info:pmid/16266986&rfr_iscdi=true |