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Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10
Summary During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on...
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| Published in: | Clinical and experimental immunology 2006-09, Vol.145 (3), p.535-544 |
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| container_end_page | 544 |
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| container_title | Clinical and experimental immunology |
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| creator | Coma, G. Peña, R. Blanco, J. Rosell, A. Borras, F. E. Esté, J. A. Clotet, B. Ruiz, L. Parkhouse, R. M. E. Bofill, M. |
| description | Summary
During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on human peripheral blood monocytes and mature bronchoalveolar lavage (BAL) macrophages. IL‐12 and IL‐18 together, but not alone, prevented spontaneous apoptosis of cultured monocytes, promoted monocyte clustering and subsequent differentiation into macrophages. These morphological changes were accompanied by increased secretion of CXC chemokine ligands (CXCL)9, CXCL10 (up to 100‐fold, P |
| doi_str_mv | 10.1111/j.1365-2249.2006.03145.x |
| format | article |
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During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on human peripheral blood monocytes and mature bronchoalveolar lavage (BAL) macrophages. IL‐12 and IL‐18 together, but not alone, prevented spontaneous apoptosis of cultured monocytes, promoted monocyte clustering and subsequent differentiation into macrophages. These morphological changes were accompanied by increased secretion of CXC chemokine ligands (CXCL)9, CXCL10 (up to 100‐fold, P < 0·001) and CXCL8 (up to 10‐fold, P < 0·001) but not CCL3, CCL4 or CCL5. Mature macrophages (from BALs) expressed high basal levels of CXCL8, that were no modified upon stimulation with IL‐12 and IL‐18. In contrast, the basal production of CXCL9 and CXCL10 by BALs was increased by 10‐fold (P < 0·001) in the presence of either IL‐12 or IL‐18 alone and by 50‐fold in the presence of both cytokines. In conclusion, our results indicate a relevant role for IL‐12 and IL‐18 in the activation and resolution of inflammatory immune responses, by increasing the survival of monocytes and by inducing the production of chemokines. In particular, those that may regulate angiogenesis and promote the recruitment of monocytes, activated T cells (CXCL9 and CXCL10) and granulocytes (CXCL8).</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.2006.03145.x</identifier><identifier>PMID: 16907924</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Analysis of Variance ; angiogenic chemokines ; Basic Immunology ; Biological and medical sciences ; bronchoalveolar macrophages ; Cell Differentiation - drug effects ; Cell Survival - drug effects ; Cells, Cultured ; Chemokine CXCL10 ; Chemokine CXCL9 ; Chemokines, CXC - biosynthesis ; cytokines ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; IL‐12 ; IL‐18 ; Immunity, Innate ; Immunopathology ; innate immunity ; Interleukin-12 - pharmacology ; Interleukin-18 - pharmacology ; Interleukin-8 ; Macrophages, Alveolar - immunology ; Medical sciences ; monocytes ; Monocytes - immunology ; Phagocytosis ; STAT4 Transcription Factor - analysis ; Stimulation, Chemical</subject><ispartof>Clinical and experimental immunology, 2006-09, Vol.145 (3), p.535-544</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Sep 2006</rights><rights>2006 British Society for Immunology 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5295-769db4929e5cda0d989c8a971e7b8d7a09d9a13522d2fee1b65c326bcbfc75a83</citedby><cites>FETCH-LOGICAL-c5295-769db4929e5cda0d989c8a971e7b8d7a09d9a13522d2fee1b65c326bcbfc75a83</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/PMC1809701/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809701/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18035529$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16907924$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Coma, G.</creatorcontrib><creatorcontrib>Peña, R.</creatorcontrib><creatorcontrib>Blanco, J.</creatorcontrib><creatorcontrib>Rosell, A.</creatorcontrib><creatorcontrib>Borras, F. E.</creatorcontrib><creatorcontrib>Esté, J. A.</creatorcontrib><creatorcontrib>Clotet, B.</creatorcontrib><creatorcontrib>Ruiz, L.</creatorcontrib><creatorcontrib>Parkhouse, R. M. E.</creatorcontrib><creatorcontrib>Bofill, M.</creatorcontrib><title>Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on human peripheral blood monocytes and mature bronchoalveolar lavage (BAL) macrophages. IL‐12 and IL‐18 together, but not alone, prevented spontaneous apoptosis of cultured monocytes, promoted monocyte clustering and subsequent differentiation into macrophages. These morphological changes were accompanied by increased secretion of CXC chemokine ligands (CXCL)9, CXCL10 (up to 100‐fold, P < 0·001) and CXCL8 (up to 10‐fold, P < 0·001) but not CCL3, CCL4 or CCL5. Mature macrophages (from BALs) expressed high basal levels of CXCL8, that were no modified upon stimulation with IL‐12 and IL‐18. In contrast, the basal production of CXCL9 and CXCL10 by BALs was increased by 10‐fold (P < 0·001) in the presence of either IL‐12 or IL‐18 alone and by 50‐fold in the presence of both cytokines. In conclusion, our results indicate a relevant role for IL‐12 and IL‐18 in the activation and resolution of inflammatory immune responses, by increasing the survival of monocytes and by inducing the production of chemokines. In particular, those that may regulate angiogenesis and promote the recruitment of monocytes, activated T cells (CXCL9 and CXCL10) and granulocytes (CXCL8).</description><subject>Analysis of Variance</subject><subject>angiogenic chemokines</subject><subject>Basic Immunology</subject><subject>Biological and medical sciences</subject><subject>bronchoalveolar macrophages</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL10</subject><subject>Chemokine CXCL9</subject><subject>Chemokines, CXC - biosynthesis</subject><subject>cytokines</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>IL‐12</subject><subject>IL‐18</subject><subject>Immunity, Innate</subject><subject>Immunopathology</subject><subject>innate immunity</subject><subject>Interleukin-12 - pharmacology</subject><subject>Interleukin-18 - pharmacology</subject><subject>Interleukin-8</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Medical sciences</subject><subject>monocytes</subject><subject>Monocytes - immunology</subject><subject>Phagocytosis</subject><subject>STAT4 Transcription Factor - analysis</subject><subject>Stimulation, Chemical</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqNksFu1DAQhiMEokvhFZCFBGqlJthO4tgHkFBUYKVIXIrEzXIcp-vFsRc72XZvPAKvwWvxJDi7qxY44Ys9nm9-z3gmSQCCGYrr9TpDOSlTjAuWYQhJBnNUlNntg2Rx53iYLCCELGUIFifJkxDW0SSE4MfJCSIMVgwXi-TnlVdiHJQdgevB4KyTu1EFcKPHFdB2VN6o6au24GzZnP_6_gNhsDFTAMtmNigIox4mI-aQMPmt3gpzATrd98pHTS1G7SwQtgPjSoGNd90k91fxsfpLDeRKDS7KK2D0dcQCOIvXzTm9mN0N24fOJwSfJo96YYJ6dtxPk8_vL6_qj2nz6cOyftekssSsTCvCurZgmKlSdgJ2jDJJBauQqlraVQKyjgmUlxh3uFcKtaSUOSatbHtZlYLmp8nbg-5magfVyViGF4ZvvB6E33EnNP_bY_WKX7stRxSyCqIo8Ooo4N23SYWRDzpIZYywyk2BE1oVtKIwgi_-Addu8jYWxxEjlOYVmyF6gKR3IXjV32WCIJ-Hga_53HM-95zPw8D3w8BvY-jzPyu5Dzx2PwIvj4AIUpjeCyt1uOdijmX81Mi9OXA32qjdfyfA68vlfMp_Az3d0lE</recordid><startdate>200609</startdate><enddate>200609</enddate><creator>Coma, G.</creator><creator>Peña, R.</creator><creator>Blanco, J.</creator><creator>Rosell, A.</creator><creator>Borras, F. E.</creator><creator>Esté, J. A.</creator><creator>Clotet, B.</creator><creator>Ruiz, L.</creator><creator>Parkhouse, R. M. E.</creator><creator>Bofill, M.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Oxford University Press</general><general>Blackwell Science Inc</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>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200609</creationdate><title>Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10</title><author>Coma, G. ; Peña, R. ; Blanco, J. ; Rosell, A. ; Borras, F. E. ; Esté, J. A. ; Clotet, B. ; Ruiz, L. ; Parkhouse, R. M. E. ; Bofill, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5295-769db4929e5cda0d989c8a971e7b8d7a09d9a13522d2fee1b65c326bcbfc75a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Analysis of Variance</topic><topic>angiogenic chemokines</topic><topic>Basic Immunology</topic><topic>Biological and medical sciences</topic><topic>bronchoalveolar macrophages</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL10</topic><topic>Chemokine CXCL9</topic><topic>Chemokines, CXC - biosynthesis</topic><topic>cytokines</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>IL‐12</topic><topic>IL‐18</topic><topic>Immunity, Innate</topic><topic>Immunopathology</topic><topic>innate immunity</topic><topic>Interleukin-12 - pharmacology</topic><topic>Interleukin-18 - pharmacology</topic><topic>Interleukin-8</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Medical sciences</topic><topic>monocytes</topic><topic>Monocytes - immunology</topic><topic>Phagocytosis</topic><topic>STAT4 Transcription Factor - analysis</topic><topic>Stimulation, Chemical</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Coma, G.</creatorcontrib><creatorcontrib>Peña, R.</creatorcontrib><creatorcontrib>Blanco, J.</creatorcontrib><creatorcontrib>Rosell, A.</creatorcontrib><creatorcontrib>Borras, F. E.</creatorcontrib><creatorcontrib>Esté, J. A.</creatorcontrib><creatorcontrib>Clotet, B.</creatorcontrib><creatorcontrib>Ruiz, L.</creatorcontrib><creatorcontrib>Parkhouse, R. M. E.</creatorcontrib><creatorcontrib>Bofill, 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><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Coma, G.</au><au>Peña, R.</au><au>Blanco, J.</au><au>Rosell, A.</au><au>Borras, F. E.</au><au>Esté, J. A.</au><au>Clotet, B.</au><au>Ruiz, L.</au><au>Parkhouse, R. M. E.</au><au>Bofill, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2006-09</date><risdate>2006</risdate><volume>145</volume><issue>3</issue><spage>535</spage><epage>544</epage><pages>535-544</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Summary
During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on human peripheral blood monocytes and mature bronchoalveolar lavage (BAL) macrophages. IL‐12 and IL‐18 together, but not alone, prevented spontaneous apoptosis of cultured monocytes, promoted monocyte clustering and subsequent differentiation into macrophages. These morphological changes were accompanied by increased secretion of CXC chemokine ligands (CXCL)9, CXCL10 (up to 100‐fold, P < 0·001) and CXCL8 (up to 10‐fold, P < 0·001) but not CCL3, CCL4 or CCL5. Mature macrophages (from BALs) expressed high basal levels of CXCL8, that were no modified upon stimulation with IL‐12 and IL‐18. In contrast, the basal production of CXCL9 and CXCL10 by BALs was increased by 10‐fold (P < 0·001) in the presence of either IL‐12 or IL‐18 alone and by 50‐fold in the presence of both cytokines. In conclusion, our results indicate a relevant role for IL‐12 and IL‐18 in the activation and resolution of inflammatory immune responses, by increasing the survival of monocytes and by inducing the production of chemokines. In particular, those that may regulate angiogenesis and promote the recruitment of monocytes, activated T cells (CXCL9 and CXCL10) and granulocytes (CXCL8).</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16907924</pmid><doi>10.1111/j.1365-2249.2006.03145.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis of Variance angiogenic chemokines Basic Immunology Biological and medical sciences bronchoalveolar macrophages Cell Differentiation - drug effects Cell Survival - drug effects Cells, Cultured Chemokine CXCL10 Chemokine CXCL9 Chemokines, CXC - biosynthesis cytokines Fundamental and applied biological sciences. Psychology Fundamental immunology Humans IL‐12 IL‐18 Immunity, Innate Immunopathology innate immunity Interleukin-12 - pharmacology Interleukin-18 - pharmacology Interleukin-8 Macrophages, Alveolar - immunology Medical sciences monocytes Monocytes - immunology Phagocytosis STAT4 Transcription Factor - analysis Stimulation, Chemical |
| title | Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10 |
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