IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M
The interleukin-1 family member IL-33 participates in both innate and adaptive T helper-2 immune cell responses in models of lung disease. The IL-6-type cytokine Oncostatin M (OSM) elevates lung inflammation, Th2-skewed cytokines, alternatively activated (M2) macrophages, and eosinophils in C57Bl/6...
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| Veröffentlicht in: | Mediators of inflammation 2020, Vol.2020 (2020), p.1-17, Article 4087315 |
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| creator | Richards, Carl D. Humbles, Allison Yip, Ashley Park, Rex Ayaub, Ehab A. Dubey, Anisha Botelho, Fernando Kolbeck, Roland |
| description | The interleukin-1 family member IL-33 participates in both innate and adaptive T helper-2 immune cell responses in models of lung disease. The IL-6-type cytokine Oncostatin M (OSM) elevates lung inflammation, Th2-skewed cytokines, alternatively activated (M2) macrophages, and eosinophils in C57Bl/6 mice in vivo. Since OSM induces IL-33 expression, we here test the IL-33 function in OSM-mediated lung inflammation using IL-33-/- mice. Adenoviral OSM (AdOSM) markedly induced IL-33 mRNA and protein levels in wild-type animals while IL-33 was undetectable in IL-33-/- animals. AdOSM treatment showed recruitment of neutrophils, eosinophils, and elevated inflammatory chemokines (KC, eotaxin-1, MIP1a, and MIP1b), Th2 cytokines (IL-4/IL-5), and arginase-1 (M2 macrophage marker) whereas these responses were markedly diminished in IL-33-/- mice. AdOSM-induced IL-33 was unaffected by IL-6-/- deficiency. AdOSM also induced IL-33R+ ILC2 cells in the lung, while IL-6 (AdIL-6) overexpression did not. Flow-sorted ILC2 responded in vitro to IL-33 (but not OSM or IL-6 stimulation). Matrix remodelling genes col3A1, MMP-13, and TIMP-1 were also decreased in IL-33-/- mice. In vitro, IL-33 upregulated expression of OSM in the RAW264.7 macrophage cell line and in bone marrow-derived macrophages. Taken together, IL-33 is a critical mediator of OSM-driven, Th2-skewed, and M2-like responses in mouse lung inflammation and contributes in part through activation of ILC2 cells. |
| doi_str_mv | 10.1155/2020/4087315 |
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The IL-6-type cytokine Oncostatin M (OSM) elevates lung inflammation, Th2-skewed cytokines, alternatively activated (M2) macrophages, and eosinophils in C57Bl/6 mice in vivo. Since OSM induces IL-33 expression, we here test the IL-33 function in OSM-mediated lung inflammation using IL-33-/- mice. Adenoviral OSM (AdOSM) markedly induced IL-33 mRNA and protein levels in wild-type animals while IL-33 was undetectable in IL-33-/- animals. AdOSM treatment showed recruitment of neutrophils, eosinophils, and elevated inflammatory chemokines (KC, eotaxin-1, MIP1a, and MIP1b), Th2 cytokines (IL-4/IL-5), and arginase-1 (M2 macrophage marker) whereas these responses were markedly diminished in IL-33-/- mice. AdOSM-induced IL-33 was unaffected by IL-6-/- deficiency. AdOSM also induced IL-33R+ ILC2 cells in the lung, while IL-6 (AdIL-6) overexpression did not. Flow-sorted ILC2 responded in vitro to IL-33 (but not OSM or IL-6 stimulation). Matrix remodelling genes col3A1, MMP-13, and TIMP-1 were also decreased in IL-33-/- mice. In vitro, IL-33 upregulated expression of OSM in the RAW264.7 macrophage cell line and in bone marrow-derived macrophages. Taken together, IL-33 is a critical mediator of OSM-driven, Th2-skewed, and M2-like responses in mouse lung inflammation and contributes in part through activation of ILC2 cells.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2020/4087315</identifier><identifier>PMID: 33376451</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antibodies ; Arginase ; Asthma ; Bone marrow ; Cell activation ; Cell Biology ; Cell culture ; Chemokines ; Collagenase 3 ; Cytokines ; Eotaxin ; Gene expression ; Hybridization ; Immunology ; Inflammation ; Interleukin 1 ; Interleukin 4 ; Interleukin 5 ; Interleukin 6 ; Interleukins ; Kinases ; Leukocytes (eosinophilic) ; Leukocytes (neutrophilic) ; Life Sciences & Biomedicine ; Lung diseases ; Lymphocytes T ; Macrophages ; Mice ; mRNA ; Oncostatin M ; Proteins ; Science & Technology ; Scientific equipment and supplies industry ; Tissue inhibitor of metalloproteinase 1</subject><ispartof>Mediators of inflammation, 2020, Vol.2020 (2020), p.1-17, Article 4087315</ispartof><rights>Copyright © 2020 Fernando Botelho et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Fernando Botelho et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Fernando Botelho et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>14</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000601119900001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c604t-520c8be301fa6362eef5ec850c913f317725149f0b0e8e54b9d216182533a5bf3</citedby><cites>FETCH-LOGICAL-c604t-520c8be301fa6362eef5ec850c913f317725149f0b0e8e54b9d216182533a5bf3</cites><orcidid>0000-0002-0081-2231 ; 0000-0002-7226-5521</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7744230/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7744230/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,879,887,2104,2116,4026,27930,27931,27932,28255,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33376451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gladue, Ronald</contributor><contributor>Ronald Gladue</contributor><creatorcontrib>Richards, Carl D.</creatorcontrib><creatorcontrib>Humbles, Allison</creatorcontrib><creatorcontrib>Yip, Ashley</creatorcontrib><creatorcontrib>Park, Rex</creatorcontrib><creatorcontrib>Ayaub, Ehab A.</creatorcontrib><creatorcontrib>Dubey, Anisha</creatorcontrib><creatorcontrib>Botelho, Fernando</creatorcontrib><creatorcontrib>Kolbeck, Roland</creatorcontrib><title>IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M</title><title>Mediators of inflammation</title><addtitle>MEDIAT INFLAMM</addtitle><addtitle>Mediators Inflamm</addtitle><description>The interleukin-1 family member IL-33 participates in both innate and adaptive T helper-2 immune cell responses in models of lung disease. The IL-6-type cytokine Oncostatin M (OSM) elevates lung inflammation, Th2-skewed cytokines, alternatively activated (M2) macrophages, and eosinophils in C57Bl/6 mice in vivo. Since OSM induces IL-33 expression, we here test the IL-33 function in OSM-mediated lung inflammation using IL-33-/- mice. Adenoviral OSM (AdOSM) markedly induced IL-33 mRNA and protein levels in wild-type animals while IL-33 was undetectable in IL-33-/- animals. AdOSM treatment showed recruitment of neutrophils, eosinophils, and elevated inflammatory chemokines (KC, eotaxin-1, MIP1a, and MIP1b), Th2 cytokines (IL-4/IL-5), and arginase-1 (M2 macrophage marker) whereas these responses were markedly diminished in IL-33-/- mice. AdOSM-induced IL-33 was unaffected by IL-6-/- deficiency. AdOSM also induced IL-33R+ ILC2 cells in the lung, while IL-6 (AdIL-6) overexpression did not. Flow-sorted ILC2 responded in vitro to IL-33 (but not OSM or IL-6 stimulation). Matrix remodelling genes col3A1, MMP-13, and TIMP-1 were also decreased in IL-33-/- mice. In vitro, IL-33 upregulated expression of OSM in the RAW264.7 macrophage cell line and in bone marrow-derived macrophages. Taken together, IL-33 is a critical mediator of OSM-driven, Th2-skewed, and M2-like responses in mouse lung inflammation and contributes in part through activation of ILC2 cells.</description><subject>Antibodies</subject><subject>Arginase</subject><subject>Asthma</subject><subject>Bone marrow</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Chemokines</subject><subject>Collagenase 3</subject><subject>Cytokines</subject><subject>Eotaxin</subject><subject>Gene expression</subject><subject>Hybridization</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Interleukin 1</subject><subject>Interleukin 4</subject><subject>Interleukin 5</subject><subject>Interleukin 6</subject><subject>Interleukins</subject><subject>Kinases</subject><subject>Leukocytes (eosinophilic)</subject><subject>Leukocytes (neutrophilic)</subject><subject>Life Sciences & Biomedicine</subject><subject>Lung diseases</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Mice</subject><subject>mRNA</subject><subject>Oncostatin M</subject><subject>Proteins</subject><subject>Science & Technology</subject><subject>Scientific equipment and supplies industry</subject><subject>Tissue inhibitor of metalloproteinase 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Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M</title><author>Richards, Carl D. ; Humbles, Allison ; Yip, Ashley ; Park, Rex ; Ayaub, Ehab A. ; Dubey, Anisha ; Botelho, Fernando ; Kolbeck, Roland</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c604t-520c8be301fa6362eef5ec850c913f317725149f0b0e8e54b9d216182533a5bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Arginase</topic><topic>Asthma</topic><topic>Bone marrow</topic><topic>Cell activation</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Chemokines</topic><topic>Collagenase 3</topic><topic>Cytokines</topic><topic>Eotaxin</topic><topic>Gene expression</topic><topic>Hybridization</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Interleukin 1</topic><topic>Interleukin 4</topic><topic>Interleukin 5</topic><topic>Interleukin 6</topic><topic>Interleukins</topic><topic>Kinases</topic><topic>Leukocytes (eosinophilic)</topic><topic>Leukocytes (neutrophilic)</topic><topic>Life Sciences & Biomedicine</topic><topic>Lung diseases</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Mice</topic><topic>mRNA</topic><topic>Oncostatin M</topic><topic>Proteins</topic><topic>Science & Technology</topic><topic>Scientific equipment and supplies industry</topic><topic>Tissue inhibitor of metalloproteinase 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Richards, Carl D.</creatorcontrib><creatorcontrib>Humbles, Allison</creatorcontrib><creatorcontrib>Yip, Ashley</creatorcontrib><creatorcontrib>Park, Rex</creatorcontrib><creatorcontrib>Ayaub, Ehab A.</creatorcontrib><creatorcontrib>Dubey, Anisha</creatorcontrib><creatorcontrib>Botelho, Fernando</creatorcontrib><creatorcontrib>Kolbeck, Roland</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa 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Ashley</au><au>Park, Rex</au><au>Ayaub, Ehab A.</au><au>Dubey, Anisha</au><au>Botelho, Fernando</au><au>Kolbeck, Roland</au><au>Gladue, Ronald</au><au>Ronald Gladue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M</atitle><jtitle>Mediators of inflammation</jtitle><stitle>MEDIAT INFLAMM</stitle><addtitle>Mediators Inflamm</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>17</epage><pages>1-17</pages><artnum>4087315</artnum><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>The interleukin-1 family member IL-33 participates in both innate and adaptive T helper-2 immune cell responses in models of lung disease. The IL-6-type cytokine Oncostatin M (OSM) elevates lung inflammation, Th2-skewed cytokines, alternatively activated (M2) macrophages, and eosinophils in C57Bl/6 mice in vivo. Since OSM induces IL-33 expression, we here test the IL-33 function in OSM-mediated lung inflammation using IL-33-/- mice. Adenoviral OSM (AdOSM) markedly induced IL-33 mRNA and protein levels in wild-type animals while IL-33 was undetectable in IL-33-/- animals. AdOSM treatment showed recruitment of neutrophils, eosinophils, and elevated inflammatory chemokines (KC, eotaxin-1, MIP1a, and MIP1b), Th2 cytokines (IL-4/IL-5), and arginase-1 (M2 macrophage marker) whereas these responses were markedly diminished in IL-33-/- mice. AdOSM-induced IL-33 was unaffected by IL-6-/- deficiency. AdOSM also induced IL-33R+ ILC2 cells in the lung, while IL-6 (AdIL-6) overexpression did not. Flow-sorted ILC2 responded in vitro to IL-33 (but not OSM or IL-6 stimulation). Matrix remodelling genes col3A1, MMP-13, and TIMP-1 were also decreased in IL-33-/- mice. In vitro, IL-33 upregulated expression of OSM in the RAW264.7 macrophage cell line and in bone marrow-derived macrophages. Taken together, IL-33 is a critical mediator of OSM-driven, Th2-skewed, and M2-like responses in mouse lung inflammation and contributes in part through activation of ILC2 cells.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33376451</pmid><doi>10.1155/2020/4087315</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-0081-2231</orcidid><orcidid>https://orcid.org/0000-0002-7226-5521</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Arginase Asthma Bone marrow Cell activation Cell Biology Cell culture Chemokines Collagenase 3 Cytokines Eotaxin Gene expression Hybridization Immunology Inflammation Interleukin 1 Interleukin 4 Interleukin 5 Interleukin 6 Interleukins Kinases Leukocytes (eosinophilic) Leukocytes (neutrophilic) Life Sciences & Biomedicine Lung diseases Lymphocytes T Macrophages Mice mRNA Oncostatin M Proteins Science & Technology Scientific equipment and supplies industry Tissue inhibitor of metalloproteinase 1 |
| title | IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-04T01%3A36%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=IL-33%20Mediates%20Lung%20Inflammation%20by%20the%20IL-6-Type%20Cytokine%20Oncostatin%20M&rft.jtitle=Mediators%20of%20inflammation&rft.au=Richards,%20Carl%20D.&rft.date=2020&rft.volume=2020&rft.issue=2020&rft.spage=1&rft.epage=17&rft.pages=1-17&rft.artnum=4087315&rft.issn=0962-9351&rft.eissn=1466-1861&rft_id=info:doi/10.1155/2020/4087315&rft_dat=%3Cgale_pubme%3EA697103541%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2474917348&rft_id=info:pmid/33376451&rft_galeid=A697103541&rft_doaj_id=oai_doaj_org_article_13b27e8ec6de4da39d57ceafb167da4f&rfr_iscdi=true |