Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis
Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)‐initiated butylated hydroxytoluene (BHT)‐promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a...
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| Veröffentlicht in: | Molecular carcinogenesis 2012-12, Vol.51 (12), p.993-1002 |
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| creator | Vikis, Haris G. Gelman, Andrew E. Franklin, Andrew Stein, Lauren Rymaszewski, Amy Zhu, Jihong Liu, Pengyuan Tichelaar, Jay W. Krupnick, Alexander S. You, Ming |
| description | Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)‐initiated butylated hydroxytoluene (BHT)‐promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor‐susceptible BALB/cByJ (BALB) mice compared to tumor‐resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte‐derived cytokine (KC)/chemokine (C‐X‐C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two‐step lung carcinogenesis model. © 2011 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/mc.20870 |
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Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)‐initiated butylated hydroxytoluene (BHT)‐promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor‐susceptible BALB/cByJ (BALB) mice compared to tumor‐resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte‐derived cytokine (KC)/chemokine (C‐X‐C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two‐step lung carcinogenesis model. © 2011 Wiley Periodicals, Inc.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.20870</identifier><identifier>PMID: 22006501</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Butylated Hydroxytoluene - toxicity ; Carcinogens - toxicity ; Cell Transformation, Neoplastic ; Female ; Flow Cytometry ; Immunologic Memory ; Immunophenotyping ; lung ; Lung cancer ; Lung Neoplasms - chemically induced ; Lung Neoplasms - immunology ; Methylcholanthrene - toxicity ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; neutrophils ; Neutrophils - immunology ; Oncology ; T cells ; T-Lymphocytes - immunology ; tumor ; Tumors</subject><ispartof>Molecular carcinogenesis, 2012-12, Vol.51 (12), p.993-1002</ispartof><rights>Copyright © 2011 Wiley Periodicals, Inc.</rights><rights>2011 WILEY PERIODICALS, INC. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5420-bd0de3680d0aa99b35d3940017fdda906af00d2686f55568c57cedf7a5f39aef3</citedby><cites>FETCH-LOGICAL-c5420-bd0de3680d0aa99b35d3940017fdda906af00d2686f55568c57cedf7a5f39aef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.20870$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.20870$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,781,785,886,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22006501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vikis, Haris G.</creatorcontrib><creatorcontrib>Gelman, Andrew E.</creatorcontrib><creatorcontrib>Franklin, Andrew</creatorcontrib><creatorcontrib>Stein, Lauren</creatorcontrib><creatorcontrib>Rymaszewski, Amy</creatorcontrib><creatorcontrib>Zhu, Jihong</creatorcontrib><creatorcontrib>Liu, Pengyuan</creatorcontrib><creatorcontrib>Tichelaar, Jay W.</creatorcontrib><creatorcontrib>Krupnick, Alexander S.</creatorcontrib><creatorcontrib>You, Ming</creatorcontrib><title>Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis</title><title>Molecular carcinogenesis</title><addtitle>Mol. Carcinog</addtitle><description>Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)‐initiated butylated hydroxytoluene (BHT)‐promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor‐susceptible BALB/cByJ (BALB) mice compared to tumor‐resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte‐derived cytokine (KC)/chemokine (C‐X‐C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two‐step lung carcinogenesis model. © 2011 Wiley Periodicals, Inc.</description><subject>Animals</subject><subject>Butylated Hydroxytoluene - toxicity</subject><subject>Carcinogens - toxicity</subject><subject>Cell Transformation, Neoplastic</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Immunologic Memory</subject><subject>Immunophenotyping</subject><subject>lung</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - chemically induced</subject><subject>Lung Neoplasms - immunology</subject><subject>Methylcholanthrene - toxicity</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Oncology</subject><subject>T cells</subject><subject>T-Lymphocytes - immunology</subject><subject>tumor</subject><subject>Tumors</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1v1DAQhi0EoktB4hegSFw4kDKOYzu-IKEVLIhShPiSerG8_ti4JPHWdqD592TZ7QoOnGx5Hj2emRehxxjOMED1otdnFTQc7qAFBtGUFa_ru2gBjRAlFg0_QQ9SugLAmFO4j06qCoBRwAsUL-yYY9i2vkuFiraI9nr00ZrChViQsre5nTrdhk4NuY12sKUffPYqW_O8WI956nbXop1MDDdTDt24Y7Yx9GH33o3DptAqaj-EzVxJPj1E95zqkn10OE_R1zevvyzflucfV--Wr85LTesKyrUBYwlrwIBSQqwJNUTU8wzcGaMEMOUATMUa5iilrNGUa2scV9QRoawjp-jl3rsd17012g45qk5uo-9VnGRQXv5bGXwrN-GnJKQRtIFZ8PQgiOF6tCnLqzDGYe5Z4rqeF40FwzP1bE_pGFKK1h1_wCB36cheyz_pzOiTvzs6grdxzEC5B375zk7_FckPy1vhgfcp25sjr-IPyTjhVH6_WMlLdvl59al-L7-R3_xeq-Y</recordid><startdate>201212</startdate><enddate>201212</enddate><creator>Vikis, Haris G.</creator><creator>Gelman, Andrew E.</creator><creator>Franklin, Andrew</creator><creator>Stein, Lauren</creator><creator>Rymaszewski, Amy</creator><creator>Zhu, Jihong</creator><creator>Liu, Pengyuan</creator><creator>Tichelaar, Jay W.</creator><creator>Krupnick, Alexander S.</creator><creator>You, Ming</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201212</creationdate><title>Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis</title><author>Vikis, Haris G. ; Gelman, Andrew E. ; Franklin, Andrew ; Stein, Lauren ; Rymaszewski, Amy ; Zhu, Jihong ; Liu, Pengyuan ; Tichelaar, Jay W. ; Krupnick, Alexander S. ; You, Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5420-bd0de3680d0aa99b35d3940017fdda906af00d2686f55568c57cedf7a5f39aef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Butylated Hydroxytoluene - toxicity</topic><topic>Carcinogens - toxicity</topic><topic>Cell Transformation, Neoplastic</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Immunologic Memory</topic><topic>Immunophenotyping</topic><topic>lung</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - chemically induced</topic><topic>Lung Neoplasms - immunology</topic><topic>Methylcholanthrene - toxicity</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Oncology</topic><topic>T cells</topic><topic>T-Lymphocytes - immunology</topic><topic>tumor</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vikis, Haris G.</creatorcontrib><creatorcontrib>Gelman, Andrew E.</creatorcontrib><creatorcontrib>Franklin, Andrew</creatorcontrib><creatorcontrib>Stein, Lauren</creatorcontrib><creatorcontrib>Rymaszewski, Amy</creatorcontrib><creatorcontrib>Zhu, Jihong</creatorcontrib><creatorcontrib>Liu, Pengyuan</creatorcontrib><creatorcontrib>Tichelaar, Jay W.</creatorcontrib><creatorcontrib>Krupnick, Alexander S.</creatorcontrib><creatorcontrib>You, Ming</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vikis, Haris G.</au><au>Gelman, Andrew E.</au><au>Franklin, Andrew</au><au>Stein, Lauren</au><au>Rymaszewski, Amy</au><au>Zhu, Jihong</au><au>Liu, Pengyuan</au><au>Tichelaar, Jay W.</au><au>Krupnick, Alexander S.</au><au>You, Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol. Carcinog</addtitle><date>2012-12</date><risdate>2012</risdate><volume>51</volume><issue>12</issue><spage>993</spage><epage>1002</epage><pages>993-1002</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)‐initiated butylated hydroxytoluene (BHT)‐promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor‐susceptible BALB/cByJ (BALB) mice compared to tumor‐resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte‐derived cytokine (KC)/chemokine (C‐X‐C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two‐step lung carcinogenesis model. © 2011 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22006501</pmid><doi>10.1002/mc.20870</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0899-1987 |
| ispartof | Molecular carcinogenesis, 2012-12, Vol.51 (12), p.993-1002 |
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| language | eng |
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| source | MEDLINE; Access via Wiley Online Library |
| subjects | Animals Butylated Hydroxytoluene - toxicity Carcinogens - toxicity Cell Transformation, Neoplastic Female Flow Cytometry Immunologic Memory Immunophenotyping lung Lung cancer Lung Neoplasms - chemically induced Lung Neoplasms - immunology Methylcholanthrene - toxicity Mice Mice, Inbred BALB C Mice, Inbred C57BL neutrophils Neutrophils - immunology Oncology T cells T-Lymphocytes - immunology tumor Tumors |
| title | Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis |
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