CC chemokine ligand-5 (CCL5/RANTES) and CC chemokine ligand-18 (CCL18/PARC) are specific markers of refractory unstable angina pectoris and are transiently raised during severe ischemic symptoms
Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP. Plasma samples of 54 patients...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2007-10, Vol.116 (17), p.1931-1941 |
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| creator | KRAAIJEVELD, A. O DE JAGER, S. C. A BIESSEN, E. A. L DE JAGER, W. J PRAKKEN, B. J MCCOLL, S. R HASPELS, I PUTTER, H VAN BERKEL, T. J. C NAGELKERKEN, L JUKEMA, J. W |
| description | Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP.
Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P |
| doi_str_mv | 10.1161/CIRCULATIONAHA.107.706986 |
| format | Article |
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Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3+ and CD14+ cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not.
We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.107.706986</identifier><identifier>PMID: 17909104</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Angina, Unstable - blood ; Angina, Unstable - pathology ; Angina, Unstable - physiopathology ; Atherosclerosis - blood ; Atherosclerosis - pathology ; Atherosclerosis - physiopathology ; Biological and medical sciences ; Blood and lymphatic vessels ; C-Reactive Protein - analysis ; Cardiology. Vascular system ; Cardiovascular system ; CD40 Ligand - blood ; Chemokine CCL5 - blood ; Chemokines, CC - blood ; Clinical Trials as Topic ; Cohort Studies ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Humans ; Leukocytes, Mononuclear - metabolism ; Leukocytes, Mononuclear - pathology ; Male ; Medical sciences ; Middle Aged ; Myocardial Ischemia - blood ; Myocardial Ischemia - pathology ; Myocardial Ischemia - physiopathology ; Pharmacology. Drug treatments ; Pneumology ; Prospective Studies ; Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases ; Receptors, CCR - metabolism ; Regeneration ; Vasodilator agents. Cerebral vasodilators</subject><ispartof>Circulation (New York, N.Y.), 2007-10, Vol.116 (17), p.1931-1941</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-dd9d9d64900520786357fe5e26662bea586069ea2189b1e79dd21ba732007dd33</citedby><cites>FETCH-LOGICAL-c470t-dd9d9d64900520786357fe5e26662bea586069ea2189b1e79dd21ba732007dd33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19194632$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17909104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KRAAIJEVELD, A. O</creatorcontrib><creatorcontrib>DE JAGER, S. C. A</creatorcontrib><creatorcontrib>BIESSEN, E. A. L</creatorcontrib><creatorcontrib>DE JAGER, W. J</creatorcontrib><creatorcontrib>PRAKKEN, B. J</creatorcontrib><creatorcontrib>MCCOLL, S. R</creatorcontrib><creatorcontrib>HASPELS, I</creatorcontrib><creatorcontrib>PUTTER, H</creatorcontrib><creatorcontrib>VAN BERKEL, T. J. C</creatorcontrib><creatorcontrib>NAGELKERKEN, L</creatorcontrib><creatorcontrib>JUKEMA, J. W</creatorcontrib><title>CC chemokine ligand-5 (CCL5/RANTES) and CC chemokine ligand-18 (CCL18/PARC) are specific markers of refractory unstable angina pectoris and are transiently raised during severe ischemic symptoms</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP.
Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3+ and CD14+ cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not.
We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses.</description><subject>Aged</subject><subject>Angina, Unstable - blood</subject><subject>Angina, Unstable - pathology</subject><subject>Angina, Unstable - physiopathology</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - pathology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>C-Reactive Protein - analysis</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>CD40 Ligand - blood</subject><subject>Chemokine CCL5 - blood</subject><subject>Chemokines, CC - blood</subject><subject>Clinical Trials as Topic</subject><subject>Cohort Studies</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Humans</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Leukocytes, Mononuclear - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Ischemia - blood</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pneumology</subject><subject>Prospective Studies</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Receptors, CCR - metabolism</subject><subject>Regeneration</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd1qGzEQhUVpady0r1DUi5b0Ym1Ju5JWl8uSNAaTFNe5XrSrWVfN_rjSuuDX65N1HBtCoVB0MWj4Zs5wDiEfOJtzrviiXK7Lh1WxWd7fFbfFnDM910yZXL0gMy5FlmQyNS_JjDFmEp0KcUHexPgDvyrV8jW54Noww1k2I7_LkjbfoR8f_QC081s7uETSq7JcycW6uNtcf_tMsUf_xfH8CeT54muxLpELQOMOGt_6hvY2PEKIdGxpgDbYZhrDge6HONm6A9y59YOlSGPfxyeN4_wU7BA9DFN3oMH6CI66ffDDlkb4BQj4eLwDBeKh301jH9-SV63tIrw710vycHO9KW-T1f2XZVmskibTbEqcM_hUZhiTgulcpVK3IEEopUQNVuYKPQQreG5qDto4J3ht0T7GtHNpekk-nfbuwvhzD3GqerwFus4OMO5jpfIsSzMh_gsKJnN0P0fQnMAmjDGiS9UuePTtUHFWHZOu_k4a27o6JY2z788i-7oH9zx5jhaBj2fAxsZ2mMDQ-PjMGW4ylYr0D5f7sq0</recordid><startdate>20071023</startdate><enddate>20071023</enddate><creator>KRAAIJEVELD, A. O</creator><creator>DE JAGER, S. C. A</creator><creator>BIESSEN, E. A. L</creator><creator>DE JAGER, W. 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Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Humans</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Leukocytes, Mononuclear - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Ischemia - blood</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pneumology</topic><topic>Prospective Studies</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</topic><topic>Receptors, CCR - metabolism</topic><topic>Regeneration</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KRAAIJEVELD, A. O</creatorcontrib><creatorcontrib>DE JAGER, S. C. A</creatorcontrib><creatorcontrib>BIESSEN, E. A. L</creatorcontrib><creatorcontrib>DE JAGER, W. J</creatorcontrib><creatorcontrib>PRAKKEN, B. J</creatorcontrib><creatorcontrib>MCCOLL, S. R</creatorcontrib><creatorcontrib>HASPELS, I</creatorcontrib><creatorcontrib>PUTTER, H</creatorcontrib><creatorcontrib>VAN BERKEL, T. J. C</creatorcontrib><creatorcontrib>NAGELKERKEN, L</creatorcontrib><creatorcontrib>JUKEMA, J. W</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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KRAAIJEVELD, A. O</au><au>DE JAGER, S. C. A</au><au>BIESSEN, E. A. L</au><au>DE JAGER, W. J</au><au>PRAKKEN, B. J</au><au>MCCOLL, S. R</au><au>HASPELS, I</au><au>PUTTER, H</au><au>VAN BERKEL, T. J. C</au><au>NAGELKERKEN, L</au><au>JUKEMA, J. W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CC chemokine ligand-5 (CCL5/RANTES) and CC chemokine ligand-18 (CCL18/PARC) are specific markers of refractory unstable angina pectoris and are transiently raised during severe ischemic symptoms</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2007-10-23</date><risdate>2007</risdate><volume>116</volume><issue>17</issue><spage>1931</spage><epage>1941</epage><pages>1931-1941</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP.
Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3+ and CD14+ cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not.
We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>17909104</pmid><doi>10.1161/CIRCULATIONAHA.107.706986</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2007-10, Vol.116 (17), p.1931-1941 |
| issn | 0009-7322 1524-4539 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Aged Angina, Unstable - blood Angina, Unstable - pathology Angina, Unstable - physiopathology Atherosclerosis - blood Atherosclerosis - pathology Atherosclerosis - physiopathology Biological and medical sciences Blood and lymphatic vessels C-Reactive Protein - analysis Cardiology. Vascular system Cardiovascular system CD40 Ligand - blood Chemokine CCL5 - blood Chemokines, CC - blood Clinical Trials as Topic Cohort Studies Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Humans Leukocytes, Mononuclear - metabolism Leukocytes, Mononuclear - pathology Male Medical sciences Middle Aged Myocardial Ischemia - blood Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Pharmacology. Drug treatments Pneumology Prospective Studies Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Receptors, CCR - metabolism Regeneration Vasodilator agents. Cerebral vasodilators |
| title | CC chemokine ligand-5 (CCL5/RANTES) and CC chemokine ligand-18 (CCL18/PARC) are specific markers of refractory unstable angina pectoris and are transiently raised during severe ischemic symptoms |
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