TY - JOUR
T1 - Effect of interleukin-10 on the production of tumor necrosis factor-alpha by peripheral blood mononuclear cells from patients with chronic heart failure
AU - Bolger, Aidan P.
AU - Sharma, Rakesh
AU - Von Haehling, Stephan
AU - Doehner, Wolfram
AU - Oliver, Brian
AU - Rauchhaus, Mathias
AU - Coats, Andrew J S
AU - Adcock, Ian M.
AU - Anker, Stefan D.
PY - 2002/8/15
Y1 - 2002/8/15
N2 - 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
AB - 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
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U2 - 10.1016/S0002-9149(02)02494-3
DO - 10.1016/S0002-9149(02)02494-3
M3 - Article
C2 - 12161227
AN - SCOPUS:0037102274
VL - 90
SP - 384
EP - 389
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 4
ER -