title: Circulating monocytes in patients with acute coronary syndromes lack sufficient interleukin-10 production after lipopolysaccharide stimulation.
abstract: Acute coronary syndromes (ACS) are associated with inflammation resulting from monocyte activation. We sought for differences in the production of pro- and anti-inflammatory cytokines by monocytes from patients with ACS. C-reactive protein (CRP) and neopterin were measured in 22 patients with acute coronary syndromes, 50 patients with stable vascular disease and 22 healthy controls. Production of tumour necrosis factor (TNF)-alpha and interleukin (IL)-10 was determined after, respectively, 6 and 24 h of incubation of full blood with lipopolysaccharide (LPS). Levels of CRP [median, interquartile range (IQR)][1.5 mg/l (0.8-4.5) ACS patient versus 2.1 (0.9-3.6) stable disease versus 0.4 (0.3-1.2) healthy controls] (P < 0.001) and neopterin [7.4 nmol/l (6.0-8.7) ACS patient versus 7.1(6.0-8.9) stable disease versus 6.4 (5.6-7.3) healthy controls] (P = 0.07) were higher in both the patient groups. IL-10 production after LPS stimulation was greatly reduced in patients with acute coronary syndromes (16 175 pg/ml, 7559-28 470 pg/ml) as opposed to patients with stable disease (28 379 pg/ml, 12 601-73 968 pg/ml) and healthy controls (63 830 pg/ml, 22 040-168 000 pg/ml) (P = 0.003). TNF-alpha production was not signi fi cantly different between the groups [7313 pg/ml (4740-12 615) ACS patient versus 11 002 (5913-14 190) stable disease versus 8229 (5225-11 364) healthy controls] (P = 0.24). Circulating monocytes in unstable coronary syndromes produce equal amounts of TNF-alpha but less IL-10 after stimulation with LPS in vitro as compared with healthy controls. We hypothesize that, in acute coronary syndromes, the production proinflammatory cytokines is not counterbalanced by anti-inflammatory cytokines such as IL-10.
authors.affiliation: Department of Cardiology, University Hospital Groningen, Groningen, the Netherlands. P.L.van.Haelst@thorax.azg.nl
authors.forename: P L
authors.initials: PL
authors.lastname: van Haelst
authors.forename: J W Cohen
authors.initials: JW
authors.lastname: Tervaert
authors.forename: J
authors.initials: J
authors.lastname: Bijzet
authors.forename: C
authors.initials: C
authors.lastname: Baljé-Volkers
authors.forename: J F
authors.initials: JF
authors.lastname: May
authors.forename: B
authors.initials: B
authors.lastname: Langeveld
authors.forename: R O B
authors.initials: RO
authors.lastname: Gans
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000276:immunology* / Q000378:metabolism; D001772:Blood Cell Count; D002097:C-Reactive Protein / Q000032:analysis; D003324:Coronary Artery Disease / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D009203:Myocardial Infarction / Q000276:immunology* / Q000378:metabolism; D019798:Neopterin / Q000097:blood; D016491:Peripheral Vascular Diseases / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D019798:Neopterin; D002097:C-Reactive Protein