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

Effect of interleukin-10 on the production of tumor necrosis factor-alpha by peripheral blood... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The American Journal of Cardiology Elsevier

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

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Abstract

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.

Journal

The American Journal of CardiologyElsevier

Published: Aug 15, 2002

References

  • Tumour necrosis factor in chronic heart failure
    Bolger, A.P.; Anker, S.D.
  • Recent insights into the role of tumor necrosis factor in the failing heart
    Mann, D.L.
  • Elevated soluble CD14 receptors and altered cytokines in chronic heart failure
    Anker, S.D.; Egerer, K.R.; Volk, H.D.; Kox, W.J.; Poole-Wilson, P.A.; Coats, A.J.
  • Clinical Trials Update. CAPRICORN, COPERNICUS, MIRACLE, STAF, RITZ-2, RECOVER and RENAISSANCE and cachexia and cholesterol in heart failure. Highlights of the Scientific Sessions of the American College of Cardiology, 2001
    Louis, A.; Cleland, J.G.; Crabbe, S.; Ford, S.; Thackray, S.; Houghton, T.; Clark, A.
  • Interleukin 10 treatment reduces fibrosis in patients with chronic hepatitis C
    Nelson, D.R.; Lauwers, G.Y.; Lau, J.Y.; Davis, G.L.
  • Cytokine generation capacities of monocytes are reduced in patients with severe heart failure
    Shimokawa, H.; Kuroiwa-Matsumoto, M.; Takeshita, A.

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