Circulating monocytes in patients with acute coronary syndromes lack sufficient interleukin-10 production after lipopolysaccharide stimulation

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)-α 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-α production was not significantly 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-α 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.