title: Circulating levels of MCP-1 and eotaxin are not associated with presence of atherosclerosis or previous myocardial infarction.
abstract: The chemokines are a family of signalling proteins that participate in regulation of the immune system and have been implicated in the pathogenesis of vascular diseases. Deleting the gene encoding the chemokine MCP-1 in mouse models of atherosclerosis reduces lipid lesion formation and circulating chemokines are upregulated in man immediately following myocardial infarction (MI) or coronary angioplasty. We have therefore investigated whether circulating levels of two chemokines (MCP-1 and eotaxin) differ between subjects with and without atherosclerosis. We have used three different methods of measuring the presence and extent of atherosclerosis in human subjects: duplex ultrasonography of the carotid arteries and clinical diagnosis of coronary heart disease on individuals from the general population and coronary angiography on patients with suspected heart disease. There was no difference in the levels of circulating MCP-1 or eotaxin, measured by ELISA, between subjects with and without atherosclerosis. Furthermore, any increase in circulating MCP-1 following acute MI must be short-lived, since chemokine levels were not different in subjects who had had an MI previously compared to those who had not. We conclude that although there may be a transient increase in circulating chemokine levels following coronary angioplasty, there is no difference in the levels of circulating MCP-1 or eotaxin in subjects with and without atherosclerosis.
authors.affiliation: Department of Medicine, University of Cambridge, Box 157, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK. david.mosedale@papworth.nhs.uk
authors.forename: David E
authors.initials: DE
authors.lastname: Mosedale
authors.forename: Duncan J
authors.initials: DJ
authors.lastname: Smith
authors.forename: Sri
authors.initials: S
authors.lastname: Aitken
authors.forename: Peter M
authors.initials: PM
authors.lastname: Schofield
authors.forename: Sarah C
authors.initials: SC
authors.lastname: Clarke
authors.forename: Duncan
authors.initials: D
authors.lastname: McNab
authors.forename: Hester
authors.initials: H
authors.lastname: Goddard
authors.forename: Catharine R
authors.initials: CR
authors.lastname: Gale
authors.forename: Christopher N
authors.initials: CN
authors.lastname: Martyn
authors.forename: Hugh W L
authors.initials: HW
authors.lastname: Bethell
authors.forename: Caryl
authors.initials: C
authors.lastname: Barnard
authors.forename: Sarah
authors.initials: S
authors.lastname: Hayns
authors.forename: Claire
authors.initials: C
authors.lastname: Nugent
authors.forename: Annik
authors.initials: A
authors.lastname: Panicker
authors.forename: David J
authors.initials: DJ
authors.lastname: Grainger
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D054413:Chemokine CCL11; D018932:Chemokine CCL2 / Q000097:blood*; D019742:Chemokines, CC / Q000097:blood*; D002631:Chemotactic Factors, Eosinophil / Q000097:blood*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000000981:diagnostic imaging; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000000981:diagnostic imaging; D011379:Prognosis; D012720:Severity of Illness Index; D018615:Ultrasonography, Doppler, Color
chemical_list: D015415:Biomarkers; C515456:CCL11 protein, human; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D018932:Chemokine CCL2; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil