Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart
Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil‐associated diseases. Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in whic...
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| Veröffentlicht in: | European journal of immunology 2016-12, Vol.46 (12), p.2749-2760 |
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| creator | Diny, Nicola L. Hou, Xuezhou Barin, Jobert G. Chen, Guobao Talor, Monica V. Schaub, Julie Russell, Stuart D. Klingel, Karin Rose, Noel R. Čiháková, Daniela |
| description | Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil‐associated diseases. Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in which experimental autoimmune myocarditis (EAM) is induced in IFNγ−/−IL‐17A−/− mice. Two conditions are necessary for efficient eosinophil trafficking to the heart: high eotaxin (CCL11, CCL24) expression in the heart and expression of the eotaxin receptor CCR3 by eosinophils. We identified cardiac fibroblasts as the source of CCL11 in the heart interstitium. CCL24 is produced by F4/80+ macrophages localized at inflammatory foci in the heart. Expression of CCL11 and CCL24 is controlled by Th2 cytokines, IL‐4 and IL‐13. To determine the relevance of this pathway in humans, we analyzed endomyocardial biopsy samples from myocarditis patients. Expression of CCL11 and CCL26 was significantly increased in eosinophilic myocarditis compared to chronic lymphocytic myocarditis and positively correlated with the number of eosinophils. Thus, eosinophil trafficking to the heart is dependent on the eotaxin‐CCR3 pathway in a mouse model of EAM and associated with cardiac eotaxin expression in patients with eosinophilic myocarditis. Blocking this pathway may prevent eosinophil‐mediated cardiac damage.
We determined the pathway for eosinophil trafficking to the heart by examining a murine myocarditis model and heart biopsies from myocarditis patients. IL‐4 and IL‐13 induce production of eotaxins CCL11 and CCL24 by cardiac fibroblasts and macrophages. In response to eotaxins, eosinophils migrate to the heart via the receptor CCR3. |
| doi_str_mv | 10.1002/eji.201646557 |
| format | Article |
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We determined the pathway for eosinophil trafficking to the heart by examining a murine myocarditis model and heart biopsies from myocarditis patients. IL‐4 and IL‐13 induce production of eotaxins CCL11 and CCL24 by cardiac fibroblasts and macrophages. In response to eotaxins, eosinophils migrate to the heart via the receptor CCR3.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.201646557</identifier><identifier>PMID: 27621211</identifier><identifier>CODEN: EJIMAF</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Adult ; Aged ; Animals ; Cardiac Myosins - immunology ; Cardiomyopathy ; Cell Movement ; Cell trafficking ; Cells, Cultured ; Chemokine CCL11 - metabolism ; Chemokine CCL24 - metabolism ; Chemokines ; Eosinophils ; Eosinophils - immunology ; Eotaxins ; Experimental autoimmune myocarditis ; Female ; Fibroblasts ; Fibroblasts - immunology ; Heart ; Humans ; Inflammation ; Interferon-gamma - genetics ; Macrophages - immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mice, Transgenic ; Mortality ; Myocarditis - immunology ; Myocardium - immunology ; Myocardium - pathology ; Nervous System Autoimmune Disease, Experimental - immunology ; Receptors, CCR3 - genetics ; Rodents ; Th1-Th2 Balance</subject><ispartof>European journal of immunology, 2016-12, Vol.46 (12), p.2749-2760</ispartof><rights>2016 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><rights>2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4915-a3193afb48c0670c3db6002339373fcfd31fe856084c5f63772ca19818234eb53</citedby><cites>FETCH-LOGICAL-c4915-a3193afb48c0670c3db6002339373fcfd31fe856084c5f63772ca19818234eb53</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%2Feji.201646557$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.201646557$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27621211$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Diny, Nicola L.</creatorcontrib><creatorcontrib>Hou, Xuezhou</creatorcontrib><creatorcontrib>Barin, Jobert G.</creatorcontrib><creatorcontrib>Chen, Guobao</creatorcontrib><creatorcontrib>Talor, Monica V.</creatorcontrib><creatorcontrib>Schaub, Julie</creatorcontrib><creatorcontrib>Russell, Stuart D.</creatorcontrib><creatorcontrib>Klingel, Karin</creatorcontrib><creatorcontrib>Rose, Noel R.</creatorcontrib><creatorcontrib>Čiháková, Daniela</creatorcontrib><title>Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil‐associated diseases. Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in which experimental autoimmune myocarditis (EAM) is induced in IFNγ−/−IL‐17A−/− mice. Two conditions are necessary for efficient eosinophil trafficking to the heart: high eotaxin (CCL11, CCL24) expression in the heart and expression of the eotaxin receptor CCR3 by eosinophils. We identified cardiac fibroblasts as the source of CCL11 in the heart interstitium. CCL24 is produced by F4/80+ macrophages localized at inflammatory foci in the heart. Expression of CCL11 and CCL24 is controlled by Th2 cytokines, IL‐4 and IL‐13. To determine the relevance of this pathway in humans, we analyzed endomyocardial biopsy samples from myocarditis patients. Expression of CCL11 and CCL26 was significantly increased in eosinophilic myocarditis compared to chronic lymphocytic myocarditis and positively correlated with the number of eosinophils. Thus, eosinophil trafficking to the heart is dependent on the eotaxin‐CCR3 pathway in a mouse model of EAM and associated with cardiac eotaxin expression in patients with eosinophilic myocarditis. Blocking this pathway may prevent eosinophil‐mediated cardiac damage.
We determined the pathway for eosinophil trafficking to the heart by examining a murine myocarditis model and heart biopsies from myocarditis patients. IL‐4 and IL‐13 induce production of eotaxins CCL11 and CCL24 by cardiac fibroblasts and macrophages. In response to eotaxins, eosinophils migrate to the heart via the receptor CCR3.</description><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Cardiac Myosins - immunology</subject><subject>Cardiomyopathy</subject><subject>Cell Movement</subject><subject>Cell trafficking</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL11 - metabolism</subject><subject>Chemokine CCL24 - metabolism</subject><subject>Chemokines</subject><subject>Eosinophils</subject><subject>Eosinophils - immunology</subject><subject>Eotaxins</subject><subject>Experimental autoimmune myocarditis</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - immunology</subject><subject>Heart</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interferon-gamma - genetics</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Mortality</subject><subject>Myocarditis - immunology</subject><subject>Myocardium - immunology</subject><subject>Myocardium - pathology</subject><subject>Nervous System Autoimmune Disease, Experimental - immunology</subject><subject>Receptors, CCR3 - genetics</subject><subject>Rodents</subject><subject>Th1-Th2 Balance</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkT1vFDEQhi0EIkegpEWWaGg2-Nu7DRKKAgQF0UBtzXrHdz721oe9S8i_x-HCCSgQlaXx48cz8xLylLMzzph4idt4Jhg3ymht75EV14I3iit-n6wY46oRXctOyKNStoyxzujuITkR1gguOF-R6w_gc9pvYI2FwjRQD3mI4GmIfU79CGWu9Yx03iDdQZzoPqdh8ZgLTYFimuF7nA5PM66XEWas1RKnKo0jnTOEEP2XOK3pnH5aNgh5fkweBBgLPrk7T8nnNxefzt81Vx_fXp6_vmq86rhuQPJOQuhV65mxzMuhN3VqKTtpZfBhkDxgqw1rldfBSGuFB961vBVSYa_lKXl18O6XfoeDx6l2NLp9jjvINy5BdH_eTHHj1umb04opYdsqeHEnyOnrgmV2u1g8jiNMmJbieKs1q_9p-R-o1MYKZW7R53-h27TkqW6iUkpbWae0lWoOVI2olIzh2Ddn7jZ9V9N3x_Qr_-z3YY_0r7grIA7AdRzx5t82d_H-su5Tyx8KnLrV</recordid><startdate>201612</startdate><enddate>201612</enddate><creator>Diny, Nicola L.</creator><creator>Hou, Xuezhou</creator><creator>Barin, Jobert G.</creator><creator>Chen, Guobao</creator><creator>Talor, Monica V.</creator><creator>Schaub, Julie</creator><creator>Russell, Stuart D.</creator><creator>Klingel, Karin</creator><creator>Rose, Noel R.</creator><creator>Čiháková, Daniela</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201612</creationdate><title>Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart</title><author>Diny, Nicola L. ; 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Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in which experimental autoimmune myocarditis (EAM) is induced in IFNγ−/−IL‐17A−/− mice. Two conditions are necessary for efficient eosinophil trafficking to the heart: high eotaxin (CCL11, CCL24) expression in the heart and expression of the eotaxin receptor CCR3 by eosinophils. We identified cardiac fibroblasts as the source of CCL11 in the heart interstitium. CCL24 is produced by F4/80+ macrophages localized at inflammatory foci in the heart. Expression of CCL11 and CCL24 is controlled by Th2 cytokines, IL‐4 and IL‐13. To determine the relevance of this pathway in humans, we analyzed endomyocardial biopsy samples from myocarditis patients. Expression of CCL11 and CCL26 was significantly increased in eosinophilic myocarditis compared to chronic lymphocytic myocarditis and positively correlated with the number of eosinophils. Thus, eosinophil trafficking to the heart is dependent on the eotaxin‐CCR3 pathway in a mouse model of EAM and associated with cardiac eotaxin expression in patients with eosinophilic myocarditis. Blocking this pathway may prevent eosinophil‐mediated cardiac damage.
We determined the pathway for eosinophil trafficking to the heart by examining a murine myocarditis model and heart biopsies from myocarditis patients. IL‐4 and IL‐13 induce production of eotaxins CCL11 and CCL24 by cardiac fibroblasts and macrophages. In response to eotaxins, eosinophils migrate to the heart via the receptor CCR3.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>27621211</pmid><doi>10.1002/eji.201646557</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Animals Cardiac Myosins - immunology Cardiomyopathy Cell Movement Cell trafficking Cells, Cultured Chemokine CCL11 - metabolism Chemokine CCL24 - metabolism Chemokines Eosinophils Eosinophils - immunology Eotaxins Experimental autoimmune myocarditis Female Fibroblasts Fibroblasts - immunology Heart Humans Inflammation Interferon-gamma - genetics Macrophages - immunology Male Mice Mice, Inbred BALB C Mice, Knockout Mice, Transgenic Mortality Myocarditis - immunology Myocardium - immunology Myocardium - pathology Nervous System Autoimmune Disease, Experimental - immunology Receptors, CCR3 - genetics Rodents Th1-Th2 Balance |
| title | Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart |
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