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. 2004 Apr;90(4):464-70.
doi: 10.1136/hrt.2002.007005.

Inflammatory mediators in chronic heart failure: an overview

Stefan D Anker  1 , Stephan von Haehling
Affiliations

Inflammatory mediators in chronic heart failure: an overview

Stefan D Anker et al. Heart. 2004 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Competing theories. Several theories to explain the cause(s) of inflammatory immune activation in CHF have been suggested. These theories may in fact complement each other. The myocardium itself is able to release pro-inflammatory cytokines, which is augmented by adrenergic stimulation. Myocardial tissue injury—for example, myocardial infarction, bacterial translocation, and peripheral tissue hypoxia—may lead to mononuclear cell activation, which eventually leads to pro-inflammatory cytokine activation. See text for details. LPS, lipopolysaccharide; LV, left ventricle; RV, right ventricle.
Figure 2
Figure 2
(A) TNFα signalling via a receptor complex comprising CD14 and toll-like receptor 4 (TLR4). Upon LPS binding to this complex, signal transduction via TLR4 leads to the activation of the transcription factor NF-κB. Therefore, IκB is cleared off the molecule. After transcription and translation, trimeric TNFα is inserted into the cell membrane. The TNFα converting enzyme (TACE) cleaves TNFα off the membrane to yield its soluble form (sTNFα). (B) IL-6 signalling via IL-6R and gp130. Only the latter has to be expressed to render the respective cell susceptible to IL-6, because soluble IL-6R can interact with membrane bound gp130. The activation of the receptor complex leads to the activation of different transcription factors, such as STAT1 and STAT3. (C) TNFα mediated effects. Several untoward effects have been implicated into the over-expression of TNFα. See text for details. gp, glycoprotein; IκB, inhibitory κB; IL, interleukin; iNOS, inducible isoform of nitric oxide synthase; LPS, lipopolysaccharide; LV, left ventricular; NF-κB, nuclear factor-κB; R, receptor; s, soluble; STAT, signal transducers and activator of transcription; TACE, TNFα converting enzyme; TNFα, tumour necrosis factor α.
Figure 3
Figure 3
Physiological role of different types of adhesion molecules. Selectins are mainly involved in leucocyte rolling on the endothelial wall. Integrins—for example, LFA-1—yield a much stronger interaction, which eventually leads to transendothelial migration. Endothelium derived NO plays another important role in mediating endothelial function. Its production by NOS from L-arginine leads to smooth muscle relaxation. cNOS, constitutive nitric oxide synthase; ICAM, intracellular adhesion molecule; LFA, lymphocyte function associated antigen; NO, nitric oxide; PECAM, platelet endothelial cell adhesion molecule.
See this image and copyright information in PMC

References

    1. Mann DL. Inflammatory mediators and the failing heart: past, present, and the foreseeable future. Circ Res 2002;91:988–98. ▸ Comprehensive up-to-date review of basic science issues in the context of cytokines in heart failure. - PubMed
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    1. Tsutamoto T, Hisanaga T, Wada A, et al. Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure. J Am Coll Cardiol 1998;31:391–8. - PubMed
    1. Anker SD, Egerer KR, Volk HD, et al. Elevated soluble CD14 receptors and altered cytokines in chronic heart failure. Am J Cardiol 1997;79:1426–30. ▸ Original publication formulating the endotoxin hypothesis. - PubMed
    1. Genth-Zotz S, von Haehling S, Bolger AP, et al. Pathophysiologic quantities of endotoxin-induced tumor necrosis factor-alpha release in whole blood from patients with chronic heart failure. Am J Cardiol 2002;90:1226–30. ▸ First study to use very small—that is, pathophysiologically relevant—concentrations of LPS to induce pro-inflammatory cytokine production in CHF. - PubMed

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