Heparin displaces interferon-γ-inducible chemokines (IP-10, I-TAC, and mig) sequestered in the vasculature and inhibits the transendothelial migration and arterial recruitment of T cells
Heparin, used clinically as an anticoagulant, also has antiinflammatory properties and has been described to inhibit interferon (IFN)-gamma responses in endothelial cells. We investigated the effects of heparin on the IFN-gamma-inducible chemokines IP-10/CXCL10, I-TAC/CXCL11, and Mig/CXCL9, which pl...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2006-09, Vol.114 (12), p.1293-1300 |
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| creator | RANJBARAN, Hooman YINONG WANG MANES, Thomas D YAKIMOV, Alexander O AKHTAR, Shamsuddin KLUGER, Martin S POBER, Jordan S TELLIDES, George |
| description | Heparin, used clinically as an anticoagulant, also has antiinflammatory properties and has been described to inhibit interferon (IFN)-gamma responses in endothelial cells. We investigated the effects of heparin on the IFN-gamma-inducible chemokines IP-10/CXCL10, I-TAC/CXCL11, and Mig/CXCL9, which play important roles in the vascular recruitment of IFN-gamma-producing Th1 cells through interactions with their cognate receptor, CXCR3.
Patients undergoing coronary artery bypass grafting were studied because coronary atherosclerosis is recognized as a Th1-type inflammatory disease and the subjects required systemic heparinization. Plasma levels of IP-10, I-TAC, and Mig increased immediately after heparin administration and diminished promptly after heparin antagonism with protamine. These effects were independent of detectable circulating IFN-gamma or the IFN-gamma inducer interleukin-12. We confirmed previous reports that heparin inhibits the IFN-gamma-dependent production of CXCR3 chemokine ligands using atherosclerotic coronary arteries in organ culture. In addition to prolonged treatment decreasing chemokine secretion, heparin rapidly displaced membrane-associated IP-10 from cultured endothelial cells that did not express CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under conditions of venular shear stress. Finally, heparin administration to immunodeficient mouse hosts decreased both the recruitment and accumulation of memory T cells within allogeneic human coronary arteries.
Besides inhibiting IFN-gamma responses, heparin has further immunomodulatory effects by competing for binding with IP-10, I-TAC, and Mig on endothelial cells. Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeutic efficacy of heparin in inflammatory arterial diseases, and nonanticoagulant heparin derivatives may represent a novel antiinflammatory strategy. |
| doi_str_mv | 10.1161/CIRCULATIONAHA.106.631457 |
| format | Article |
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Patients undergoing coronary artery bypass grafting were studied because coronary atherosclerosis is recognized as a Th1-type inflammatory disease and the subjects required systemic heparinization. Plasma levels of IP-10, I-TAC, and Mig increased immediately after heparin administration and diminished promptly after heparin antagonism with protamine. These effects were independent of detectable circulating IFN-gamma or the IFN-gamma inducer interleukin-12. We confirmed previous reports that heparin inhibits the IFN-gamma-dependent production of CXCR3 chemokine ligands using atherosclerotic coronary arteries in organ culture. In addition to prolonged treatment decreasing chemokine secretion, heparin rapidly displaced membrane-associated IP-10 from cultured endothelial cells that did not express CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under conditions of venular shear stress. Finally, heparin administration to immunodeficient mouse hosts decreased both the recruitment and accumulation of memory T cells within allogeneic human coronary arteries.
Besides inhibiting IFN-gamma responses, heparin has further immunomodulatory effects by competing for binding with IP-10, I-TAC, and Mig on endothelial cells. Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeutic efficacy of heparin in inflammatory arterial diseases, and nonanticoagulant heparin derivatives may represent a novel antiinflammatory strategy.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.106.631457</identifier><identifier>PMID: 16940188</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Anti-Inflammatory Agents - metabolism ; Anti-Inflammatory Agents - pharmacology ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Blood. Blood coagulation. Reticuloendothelial system ; Cardiology. Vascular system ; Cell Movement - drug effects ; Cells, Cultured ; Chemokine CXCL10 ; Chemokine CXCL11 ; Chemokine CXCL9 ; Chemokines - metabolism ; Chemokines, CXC - metabolism ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - pathology ; Coronary Vessels - drug effects ; Coronary Vessels - metabolism ; Coronary Vessels - pathology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Fundamental and applied biological sciences. Psychology ; Heparin - metabolism ; Heparin - pharmacology ; Heparin Antagonists - pharmacology ; Humans ; Interferon-gamma - metabolism ; Interleukin-12 - metabolism ; Medical sciences ; Pharmacology. Drug treatments ; Protamines - pharmacology ; Protein Binding ; Receptors, Chemokine - drug effects ; Receptors, Chemokine - metabolism ; Receptors, CXCR3 ; T-Lymphocytes - drug effects ; T-Lymphocytes - metabolism ; T-Lymphocytes - pathology ; Th1 Cells - metabolism ; Th1 Cells - pathology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 2006-09, Vol.114 (12), p.1293-1300</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-3be9433c35d1739b76cb927178f8f6d6b112173c211e7e5305a09c1748e6d54f3</citedby><cites>FETCH-LOGICAL-c483t-3be9433c35d1739b76cb927178f8f6d6b112173c211e7e5305a09c1748e6d54f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18146294$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16940188$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RANJBARAN, Hooman</creatorcontrib><creatorcontrib>YINONG WANG</creatorcontrib><creatorcontrib>MANES, Thomas D</creatorcontrib><creatorcontrib>YAKIMOV, Alexander O</creatorcontrib><creatorcontrib>AKHTAR, Shamsuddin</creatorcontrib><creatorcontrib>KLUGER, Martin S</creatorcontrib><creatorcontrib>POBER, Jordan S</creatorcontrib><creatorcontrib>TELLIDES, George</creatorcontrib><title>Heparin displaces interferon-γ-inducible chemokines (IP-10, I-TAC, and mig) sequestered in the vasculature and inhibits the transendothelial migration and arterial recruitment of T cells</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Heparin, used clinically as an anticoagulant, also has antiinflammatory properties and has been described to inhibit interferon (IFN)-gamma responses in endothelial cells. We investigated the effects of heparin on the IFN-gamma-inducible chemokines IP-10/CXCL10, I-TAC/CXCL11, and Mig/CXCL9, which play important roles in the vascular recruitment of IFN-gamma-producing Th1 cells through interactions with their cognate receptor, CXCR3.
Patients undergoing coronary artery bypass grafting were studied because coronary atherosclerosis is recognized as a Th1-type inflammatory disease and the subjects required systemic heparinization. Plasma levels of IP-10, I-TAC, and Mig increased immediately after heparin administration and diminished promptly after heparin antagonism with protamine. These effects were independent of detectable circulating IFN-gamma or the IFN-gamma inducer interleukin-12. We confirmed previous reports that heparin inhibits the IFN-gamma-dependent production of CXCR3 chemokine ligands using atherosclerotic coronary arteries in organ culture. In addition to prolonged treatment decreasing chemokine secretion, heparin rapidly displaced membrane-associated IP-10 from cultured endothelial cells that did not express CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under conditions of venular shear stress. Finally, heparin administration to immunodeficient mouse hosts decreased both the recruitment and accumulation of memory T cells within allogeneic human coronary arteries.
Besides inhibiting IFN-gamma responses, heparin has further immunomodulatory effects by competing for binding with IP-10, I-TAC, and Mig on endothelial cells. Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeutic efficacy of heparin in inflammatory arterial diseases, and nonanticoagulant heparin derivatives may represent a novel antiinflammatory strategy.</description><subject>Anti-Inflammatory Agents - metabolism</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Cardiology. Vascular system</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL10</subject><subject>Chemokine CXCL11</subject><subject>Chemokine CXCL9</subject><subject>Chemokines - metabolism</subject><subject>Chemokines, CXC - metabolism</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary Artery Disease - pathology</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - pathology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heparin - metabolism</subject><subject>Heparin - pharmacology</subject><subject>Heparin Antagonists - pharmacology</subject><subject>Humans</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-12 - metabolism</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Protamines - pharmacology</subject><subject>Protein Binding</subject><subject>Receptors, Chemokine - drug effects</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Receptors, CXCR3</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - metabolism</subject><subject>T-Lymphocytes - pathology</subject><subject>Th1 Cells - metabolism</subject><subject>Th1 Cells - pathology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGO0zAQhi0EYsvCKyBzAIG0KZ44sZ1jFAGtVLEIdc-R40yoIXGKnSDxXBx5B54JN6204sTJmplvftv_T8gLYGsAAW-r7efqblfut7cfy025BibWgkOWywdkBXmaJVnOi4dkxRgrEsnT9Io8CeFrLAWX-WNyBaLIGCi1Ir83eNTeOtracOy1wUCtm9B36EeX_PmVWNfOxjY9UnPAYfxmXURebz8lwG7oNtmX1Q3VrqWD_fKGBvw-Y4jr2EYZOh2Q_tDBzL2eZo8LZ93BNnYKy3Dy2gV07RiL3ur-pOL1ZEe3sNpHqVPbo_GznQZ0Ex07uqcG-z48JY863Qd8djmvyd37d_tqk-xuP2yrcpeYTPEp4Q0WGeeG5y1IXjRSmKZIJUjVqU60ogFI48CkACgx5yzXrDAgM4WizbOOX5NXZ92jH5f_1YMNpxdoh-McaqGUyCTAf8GUyULxBSzOoPFjCB67-ujtoP3PGlh9irj-N-LYFvU54rj7_HLJ3AzY3m9eMo3AywsQrdd9Fz02NtxzCjKRRkf-AsX4s2g</recordid><startdate>20060919</startdate><enddate>20060919</enddate><creator>RANJBARAN, Hooman</creator><creator>YINONG WANG</creator><creator>MANES, Thomas D</creator><creator>YAKIMOV, Alexander O</creator><creator>AKHTAR, Shamsuddin</creator><creator>KLUGER, Martin S</creator><creator>POBER, Jordan S</creator><creator>TELLIDES, George</creator><general>Lippincott Williams & Wilkins</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>H94</scope><scope>7X8</scope></search><sort><creationdate>20060919</creationdate><title>Heparin displaces interferon-γ-inducible chemokines (IP-10, I-TAC, and mig) sequestered in the vasculature and inhibits the transendothelial migration and arterial recruitment of T cells</title><author>RANJBARAN, Hooman ; YINONG WANG ; MANES, Thomas D ; YAKIMOV, Alexander O ; AKHTAR, Shamsuddin ; KLUGER, Martin S ; POBER, Jordan S ; TELLIDES, George</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-3be9433c35d1739b76cb927178f8f6d6b112173c211e7e5305a09c1748e6d54f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anti-Inflammatory Agents - metabolism</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Cardiology. Vascular system</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL10</topic><topic>Chemokine CXCL11</topic><topic>Chemokine CXCL9</topic><topic>Chemokines - metabolism</topic><topic>Chemokines, CXC - metabolism</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Coronary Artery Disease - pathology</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - pathology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heparin - metabolism</topic><topic>Heparin - pharmacology</topic><topic>Heparin Antagonists - pharmacology</topic><topic>Humans</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-12 - metabolism</topic><topic>Medical sciences</topic><topic>Pharmacology. 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We investigated the effects of heparin on the IFN-gamma-inducible chemokines IP-10/CXCL10, I-TAC/CXCL11, and Mig/CXCL9, which play important roles in the vascular recruitment of IFN-gamma-producing Th1 cells through interactions with their cognate receptor, CXCR3.
Patients undergoing coronary artery bypass grafting were studied because coronary atherosclerosis is recognized as a Th1-type inflammatory disease and the subjects required systemic heparinization. Plasma levels of IP-10, I-TAC, and Mig increased immediately after heparin administration and diminished promptly after heparin antagonism with protamine. These effects were independent of detectable circulating IFN-gamma or the IFN-gamma inducer interleukin-12. We confirmed previous reports that heparin inhibits the IFN-gamma-dependent production of CXCR3 chemokine ligands using atherosclerotic coronary arteries in organ culture. In addition to prolonged treatment decreasing chemokine secretion, heparin rapidly displaced membrane-associated IP-10 from cultured endothelial cells that did not express CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under conditions of venular shear stress. Finally, heparin administration to immunodeficient mouse hosts decreased both the recruitment and accumulation of memory T cells within allogeneic human coronary arteries.
Besides inhibiting IFN-gamma responses, heparin has further immunomodulatory effects by competing for binding with IP-10, I-TAC, and Mig on endothelial cells. Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeutic efficacy of heparin in inflammatory arterial diseases, and nonanticoagulant heparin derivatives may represent a novel antiinflammatory strategy.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>16940188</pmid><doi>10.1161/CIRCULATIONAHA.106.631457</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - pharmacology Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Blood. Blood coagulation. Reticuloendothelial system Cardiology. Vascular system Cell Movement - drug effects Cells, Cultured Chemokine CXCL10 Chemokine CXCL11 Chemokine CXCL9 Chemokines - metabolism Chemokines, CXC - metabolism Coronary Artery Disease - metabolism Coronary Artery Disease - pathology Coronary Vessels - drug effects Coronary Vessels - metabolism Coronary Vessels - pathology Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Fundamental and applied biological sciences. Psychology Heparin - metabolism Heparin - pharmacology Heparin Antagonists - pharmacology Humans Interferon-gamma - metabolism Interleukin-12 - metabolism Medical sciences Pharmacology. Drug treatments Protamines - pharmacology Protein Binding Receptors, Chemokine - drug effects Receptors, Chemokine - metabolism Receptors, CXCR3 T-Lymphocytes - drug effects T-Lymphocytes - metabolism T-Lymphocytes - pathology Th1 Cells - metabolism Th1 Cells - pathology Vertebrates: cardiovascular system |
| title | Heparin displaces interferon-γ-inducible chemokines (IP-10, I-TAC, and mig) sequestered in the vasculature and inhibits the transendothelial migration and arterial recruitment of T cells |
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