Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway
Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristic...
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| description | Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation. |
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Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0107063</identifier><identifier>PMID: 25198511</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptive immunity ; Animals ; Biology and Life Sciences ; Blotting, Western ; CD163 antigen ; Cell culture ; Cells, Cultured ; Cigarette smoke ; Cigarette smoking ; Cigarettes ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Drug dosages ; Epigenetics ; Flow Cytometry ; Gene expression ; Genotype & phenotype ; Immunity ; Immunosuppression ; In vivo methods and tests ; Interleukin 10 ; Interleukin 12 ; Interleukin 6 ; Janus kinase 2 ; Janus Kinase 2 - genetics ; Janus Kinase 2 - metabolism ; Laboratories ; Lung cancer ; Lung diseases ; Lungs ; Macrophages ; Macrophages, Alveolar - cytology ; Macrophages, Alveolar - drug effects ; Macrophages, Alveolar - metabolism ; Male ; Medical prognosis ; Medical schools ; Medicine ; Mice ; Mice, Inbred BALB C ; mRNA ; Neutrophils ; Nicotiana - chemistry ; Nitric oxide ; Nitric-oxide synthase ; Oxygen ; Phagocytes ; Phenotypes ; Phosphorylation ; Phosphorylation - drug effects ; Plant Extracts - pharmacology ; Polarization ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Rodents ; Signal Transduction - drug effects ; Smoke ; Smoking ; Stat3 protein ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; Transforming growth factor-b1 ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2014-09, Vol.9 (9), p.e107063-e107063</ispartof><rights>2014 Yuan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Yuan et al 2014 Yuan et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-d8771336103a14d030bae5f514bd1f7d1b9a87dc0e35869449524e4def26847c3</citedby><cites>FETCH-LOGICAL-c592t-d8771336103a14d030bae5f514bd1f7d1b9a87dc0e35869449524e4def26847c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157812/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157812/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25198511$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Fengjiao</creatorcontrib><creatorcontrib>Fu, Xiao</creatorcontrib><creatorcontrib>Shi, Hengfei</creatorcontrib><creatorcontrib>Chen, Guopu</creatorcontrib><creatorcontrib>Dong, Ping</creatorcontrib><creatorcontrib>Zhang, Weiyun</creatorcontrib><title>Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.</description><subject>Adaptive immunity</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Blotting, Western</subject><subject>CD163 antigen</subject><subject>Cell culture</subject><subject>Cells, Cultured</subject><subject>Cigarette smoke</subject><subject>Cigarette smoking</subject><subject>Cigarettes</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Drug dosages</subject><subject>Epigenetics</subject><subject>Flow Cytometry</subject><subject>Gene expression</subject><subject>Genotype & phenotype</subject><subject>Immunity</subject><subject>Immunosuppression</subject><subject>In vivo methods and tests</subject><subject>Interleukin 10</subject><subject>Interleukin 12</subject><subject>Interleukin 6</subject><subject>Janus kinase 2</subject><subject>Janus Kinase 2 - genetics</subject><subject>Janus Kinase 2 - metabolism</subject><subject>Laboratories</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Macrophages</subject><subject>Macrophages, Alveolar - cytology</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>mRNA</subject><subject>Neutrophils</subject><subject>Nicotiana - chemistry</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Oxygen</subject><subject>Phagocytes</subject><subject>Phenotypes</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Plant Extracts - pharmacology</subject><subject>Polarization</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Smoke</subject><subject>Smoking</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Transforming growth factor-b1</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIlsI_QGCJC5fdevyRxBekVcXHQhEHlrM1sSe7WZI4dZLC8utJd7dVizjZ8rz3Zub5JclL4HOQGZxvwxhbrOddaGnOgWc8lY-SUzBSzFLB5eN795PkWd9vOdcyT9OnyYnQYHINcJr4ZetHN1ShZaFkzRirlliDLoZug2tiXwXrQo2x-oN7ULFjrlpjpGEg1jfhJzH6PUR0A7uukA0bYp8XX8T599ViJVmHw-YX7p4nT0qse3pxPM-SHx_ery4-zS6_fVxeLC5nThsxzHyeZSBlClwiKM8lL5B0qUEVHsrMQ2Ewz7zjJHWeGqWMFoqUp1KkucqcPEteH3S7OvT2aFBvQac8F2AgnxDLA8IH3NouVg3GnQ1Y2f1DiGuLcahcTVZonHoKk4FTypcGFShR6JxgMtQYP2m9O3Ybi4a8o3byoX4g-rDSVhu7DtdWgc5yEJPA26NADFcj9YNtqt5RXWNLYdzPDSqTkyUT9M0_0P9vpw6o6fv6PlJ5NwxwexOaW5a9CY09hmaivbq_yB3pNiXyLyISvrI</recordid><startdate>20140908</startdate><enddate>20140908</enddate><creator>Yuan, Fengjiao</creator><creator>Fu, Xiao</creator><creator>Shi, Hengfei</creator><creator>Chen, Guopu</creator><creator>Dong, Ping</creator><creator>Zhang, Weiyun</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140908</creationdate><title>Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway</title><author>Yuan, Fengjiao ; Fu, Xiao ; Shi, Hengfei ; Chen, Guopu ; Dong, Ping ; Zhang, Weiyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-d8771336103a14d030bae5f514bd1f7d1b9a87dc0e35869449524e4def26847c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adaptive immunity</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Blotting, Western</topic><topic>CD163 antigen</topic><topic>Cell culture</topic><topic>Cells, Cultured</topic><topic>Cigarette smoke</topic><topic>Cigarette smoking</topic><topic>Cigarettes</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Drug dosages</topic><topic>Epigenetics</topic><topic>Flow Cytometry</topic><topic>Gene expression</topic><topic>Genotype & phenotype</topic><topic>Immunity</topic><topic>Immunosuppression</topic><topic>In vivo methods and tests</topic><topic>Interleukin 10</topic><topic>Interleukin 12</topic><topic>Interleukin 6</topic><topic>Janus kinase 2</topic><topic>Janus Kinase 2 - genetics</topic><topic>Janus Kinase 2 - metabolism</topic><topic>Laboratories</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Macrophages</topic><topic>Macrophages, Alveolar - cytology</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>mRNA</topic><topic>Neutrophils</topic><topic>Nicotiana - chemistry</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Oxygen</topic><topic>Phagocytes</topic><topic>Phenotypes</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Plant Extracts - pharmacology</topic><topic>Polarization</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Smoke</topic><topic>Smoking</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Transforming growth factor-b1</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Fengjiao</creatorcontrib><creatorcontrib>Fu, Xiao</creatorcontrib><creatorcontrib>Shi, Hengfei</creatorcontrib><creatorcontrib>Chen, Guopu</creatorcontrib><creatorcontrib>Dong, Ping</creatorcontrib><creatorcontrib>Zhang, Weiyun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Fengjiao</au><au>Fu, Xiao</au><au>Shi, Hengfei</au><au>Chen, Guopu</au><au>Dong, Ping</au><au>Zhang, Weiyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-09-08</date><risdate>2014</risdate><volume>9</volume><issue>9</issue><spage>e107063</spage><epage>e107063</epage><pages>e107063-e107063</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25198511</pmid><doi>10.1371/journal.pone.0107063</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2014-09, Vol.9 (9), p.e107063-e107063 |
| issn | 1932-6203 1932-6203 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adaptive immunity Animals Biology and Life Sciences Blotting, Western CD163 antigen Cell culture Cells, Cultured Cigarette smoke Cigarette smoking Cigarettes Cytokines Cytokines - genetics Cytokines - metabolism Drug dosages Epigenetics Flow Cytometry Gene expression Genotype & phenotype Immunity Immunosuppression In vivo methods and tests Interleukin 10 Interleukin 12 Interleukin 6 Janus kinase 2 Janus Kinase 2 - genetics Janus Kinase 2 - metabolism Laboratories Lung cancer Lung diseases Lungs Macrophages Macrophages, Alveolar - cytology Macrophages, Alveolar - drug effects Macrophages, Alveolar - metabolism Male Medical prognosis Medical schools Medicine Mice Mice, Inbred BALB C mRNA Neutrophils Nicotiana - chemistry Nitric oxide Nitric-oxide synthase Oxygen Phagocytes Phenotypes Phosphorylation Phosphorylation - drug effects Plant Extracts - pharmacology Polarization Reactive oxygen species Reactive Oxygen Species - metabolism Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Rodents Signal Transduction - drug effects Smoke Smoking Stat3 protein STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Transforming growth factor-b1 Tumor necrosis factor-α |
| title | Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T03%3A50%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Induction%20of%20murine%20macrophage%20M2%20polarization%20by%20cigarette%20smoke%20extract%20via%20the%20JAK2/STAT3%20pathway&rft.jtitle=PloS%20one&rft.au=Yuan,%20Fengjiao&rft.date=2014-09-08&rft.volume=9&rft.issue=9&rft.spage=e107063&rft.epage=e107063&rft.pages=e107063-e107063&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0107063&rft_dat=%3Cproquest_plos_%3E3426352611%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1560821918&rft_id=info:pmid/25198511&rft_doaj_id=oai_doaj_org_article_25af7d2971c44df9a4142b58e120399d&rfr_iscdi=true |