Effect of interleukin-10 on the production of tumor necrosis factor-alpha by peripheral blood mononuclear cells from patients with chronic heart failure

Aidan P. Bolger, Rakesh Sharma, Stephan von Haehling, Wolfram Doehner, Brian Oliver, Mathias Rauchhaus, Andrew J. S. Coats, Ian M. Adcock, Stefan D. Anker

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Chronic heart failure (HF) is a state of inflammatory immune activation characterized by elevated circulating levels of tumor necrosis factor-α (TNF-α). Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine that inhibits TNF-α production and lessens endotoxin bioactivity. It is not known whether IL-10 reduces lipopolysaccharide (LPS) stimulated TNF-α production of peripheral blood mononuclear cells (PBMCs) from patients with chronic HF. PBMCs were isolated from 15 patients with chronic HF (New York Heart Association functional class 3.0 ± 0.2, left ventricular ejection fraction 30 ± 2%, peak oxygen consumption 18.1 ± 0.8 ml/kg/min) and 15 healthy control subjects and stimulated with 1 and 10 ng/ml LPS for 24 hours with or without prior addition of IL-10 (10 ng/ml). TNF-α was quantified in cell-free supernatants by an enzyme-linked immunosorbent assay. TNF-α, soluble TNF receptors, IL-10, and LPS were quantified in plasma. LPS stimulated TNF-α production was highest in those patients in New York Heart Association class II (p <0.01 vs New York Heart Association class III and IV, p <0.001 vs control subjects). IL-10 reduced PBMC TNF-α production in all stimulated samples at 1 and 10 ng/ml LPS (mean reduction 43% at 1 ng/ml, p <0.01 and 55% at 10 ng/ml, p <0.0001). The percentage reduction in TNF-α release did not differ significantly between patients and control subjects or with respect to severity of chronic HF or baseline immune parameters. Independently of clinical severity, IL-10 profoundly inhibits TNF-α release from PBMCs isolated from patients with chronic HF. IL-10 is, therefore, a potential therapy for use in chronic HF associated with inflammatory immune activation.
Original languageEnglish
Pages (from-to)384-389
Number of pages6
JournalAmerican Journal of Cardiology
Issue number4
Publication statusPublished - 15 Aug 2002

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