Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung
High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter
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| Veröffentlicht in: | The European respiratory journal 2006-08, Vol.28 (2), p.275-285 |
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| container_title | The European respiratory journal |
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| creator | Andre, E Stoeger, T Takenaka, S Bahnweg, M Ritter, B Karg, E Lentner, B Reinhard, C Schulz, H Wjst, M |
| description | High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter |
| doi_str_mv | 10.1183/09031936.06.00071205 |
| format | Article |
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It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach. Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 microg x m(-3)) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation. Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6-1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells. In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.</description><identifier>ISSN: 0903-1936</identifier><identifier>EISSN: 1399-3003</identifier><identifier>DOI: 10.1183/09031936.06.00071205</identifier><identifier>PMID: 16641123</identifier><language>eng</language><publisher>Leeds: Eur Respiratory Soc</publisher><subject>Air Pollutants - adverse effects ; Animals ; Biological and medical sciences ; Carbon - administration & dosage ; Carbon - toxicity ; Female ; Inhalation Exposure - adverse effects ; Macrophages, Alveolar - metabolism ; Macrophages, Alveolar - pathology ; Medical sciences ; Mice ; Particle Size ; Pneumology ; Pneumonia - etiology ; Pneumonia - metabolism ; Pneumonia - pathology ; Time Factors ; Up-Regulation</subject><ispartof>The European respiratory journal, 2006-08, Vol.28 (2), p.275-285</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-9d7df05d10b9b13332860fe027fcae0437317498506cfff666f163e35dfafe313</citedby><cites>FETCH-LOGICAL-c411t-9d7df05d10b9b13332860fe027fcae0437317498506cfff666f163e35dfafe313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17986630$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16641123$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Andre, E</creatorcontrib><creatorcontrib>Stoeger, T</creatorcontrib><creatorcontrib>Takenaka, S</creatorcontrib><creatorcontrib>Bahnweg, M</creatorcontrib><creatorcontrib>Ritter, B</creatorcontrib><creatorcontrib>Karg, E</creatorcontrib><creatorcontrib>Lentner, B</creatorcontrib><creatorcontrib>Reinhard, C</creatorcontrib><creatorcontrib>Schulz, H</creatorcontrib><creatorcontrib>Wjst, M</creatorcontrib><title>Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung</title><title>The European respiratory journal</title><addtitle>Eur Respir J</addtitle><description>High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach. Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 microg x m(-3)) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation. Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6-1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells. In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.</description><subject>Air Pollutants - adverse effects</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carbon - administration & dosage</subject><subject>Carbon - toxicity</subject><subject>Female</subject><subject>Inhalation Exposure - adverse effects</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Macrophages, Alveolar - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Particle Size</subject><subject>Pneumology</subject><subject>Pneumonia - etiology</subject><subject>Pneumonia - metabolism</subject><subject>Pneumonia - pathology</subject><subject>Time Factors</subject><subject>Up-Regulation</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtrwzAQhEVpadLHPyhFlx6d7npt2T6W0BcUemnPQpalWEV-IDmU_Ps6JCUwsOzyzbAMY3cIK8SSHqECworECmYBFJhCfsaWSFWVEACds-UeSfbMgl3F-AOAIiO8ZAsUIkNMacnse98qryY39HywfOunoKzrDdcq1PNtVGFy2pvIp-A2GxMir93Yqug0H8OQuN561XVqGsKOBxPHoY-Gu55PreHdsJ0Xv-03N-zCKh_N7XFes--X56_1W_Lx-fq-fvpI9PzPlFRN0VjIG4S6qpGI0lKANZAWVisDGRWERVaVOQhtrRVCWBRkKG-ssoaQrll2yNVhiDEYK8fgOhV2EkHua5P_tUmYdaxttt0fbOO27kxzMh17moGHI6CiVt4G1WsXT1xRlUIQnLjWbdpfF4yMnfJ-jkVpwk9aylSmRU5_FF-Dbg</recordid><startdate>20060801</startdate><enddate>20060801</enddate><creator>Andre, E</creator><creator>Stoeger, T</creator><creator>Takenaka, S</creator><creator>Bahnweg, M</creator><creator>Ritter, B</creator><creator>Karg, E</creator><creator>Lentner, B</creator><creator>Reinhard, C</creator><creator>Schulz, H</creator><creator>Wjst, M</creator><general>Eur Respiratory Soc</general><general>Maney</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></search><sort><creationdate>20060801</creationdate><title>Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung</title><author>Andre, E ; Stoeger, T ; Takenaka, S ; Bahnweg, M ; Ritter, B ; Karg, E ; Lentner, B ; Reinhard, C ; Schulz, H ; Wjst, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-9d7df05d10b9b13332860fe027fcae0437317498506cfff666f163e35dfafe313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Air Pollutants - adverse effects</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carbon - administration & dosage</topic><topic>Carbon - toxicity</topic><topic>Female</topic><topic>Inhalation Exposure - adverse effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Macrophages, Alveolar - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Particle Size</topic><topic>Pneumology</topic><topic>Pneumonia - etiology</topic><topic>Pneumonia - metabolism</topic><topic>Pneumonia - pathology</topic><topic>Time Factors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andre, E</creatorcontrib><creatorcontrib>Stoeger, T</creatorcontrib><creatorcontrib>Takenaka, S</creatorcontrib><creatorcontrib>Bahnweg, M</creatorcontrib><creatorcontrib>Ritter, B</creatorcontrib><creatorcontrib>Karg, E</creatorcontrib><creatorcontrib>Lentner, B</creatorcontrib><creatorcontrib>Reinhard, C</creatorcontrib><creatorcontrib>Schulz, H</creatorcontrib><creatorcontrib>Wjst, M</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><jtitle>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andre, E</au><au>Stoeger, T</au><au>Takenaka, S</au><au>Bahnweg, M</au><au>Ritter, B</au><au>Karg, E</au><au>Lentner, B</au><au>Reinhard, C</au><au>Schulz, H</au><au>Wjst, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung</atitle><jtitle>The European respiratory journal</jtitle><addtitle>Eur Respir J</addtitle><date>2006-08-01</date><risdate>2006</risdate><volume>28</volume><issue>2</issue><spage>275</spage><epage>285</epage><pages>275-285</pages><issn>0903-1936</issn><eissn>1399-3003</eissn><abstract>High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach. Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 microg x m(-3)) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation. Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6-1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells. In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.</abstract><cop>Leeds</cop><pub>Eur Respiratory Soc</pub><pmid>16641123</pmid><doi>10.1183/09031936.06.00071205</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Air Pollutants - adverse effects Animals Biological and medical sciences Carbon - administration & dosage Carbon - toxicity Female Inhalation Exposure - adverse effects Macrophages, Alveolar - metabolism Macrophages, Alveolar - pathology Medical sciences Mice Particle Size Pneumology Pneumonia - etiology Pneumonia - metabolism Pneumonia - pathology Time Factors Up-Regulation |
| title | Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung |
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