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European Journal of Heart Failure 2003 5(4):435-442; doi:10.1016/S1388-9842(03)00002-3
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© 2003 European Society of Cardiology

Pulmonary endothelium as a site of synthesis and storage of interleukin-6 in experimental congestive heart failure

Roger Gaertnera, Delphine Lepailleur-Enoufa, Walter Gonzaleza, Antonino Nicolettib, Chantal Mandetb, Monique Philippea, Jean-Jacques Mercadiera and Jean-Baptiste Michela,*

a INSERM U460, Cardiovascular Remodelling, CHU Xavier-Bichat 16 rue Henri Huchard, 75018 Paris, France
b U430, Hôpital Broussais Paris, France

* Corresponding author. Tel.: +33-1-44-85-61-60; fax: +33-1-44-85-61-57 E-mail address: u460{at}bichat.inserm.fr


  Abstract

Background: Pulmonary endothelium is an early upstream hemodynamic target of left ventricular dysfunction. Interleukin 6 (IL-6) is a pro-inflammatory cytokine reported to increase in congestive heart failure (CHF) patients.

Aims: We sought to determine the origin of IL-6, IL-6 receptor (IL-6R) and gp130 in experimental CHF.

Methods: We used rats with coronary artery ligation as an experimental model of either compensated or decompensated heart failure. Lung and aorta samples were analysed by RT-PCR, ELISA and immunohistochemistry for IL-6 and its receptors.

Results: IL-6 mRNA expression increased in the lung of rats with decompensated heart failure and was positively correlated with infarct severity whereas IL-6R mRNA decreased in the lung of myocardial infarction rats and gp130 mRNA remained unchanged. In contrast, there were no changes in IL-6 mRNA expression in the aorta and left ventricular myocardium. IL-6 peptide content as determined by ELISA and Western Blot in lung tissue was 2-fold higher in decompensated heart failure as compared to control rats. These data were confirmed by immunohistochemistry showing a preferential endothelial localization of IL-6 in the CHF lung. IL-6 peptide was also present in the pleural effusion of decompensated heart failure and was positively correlated with IL-6 mRNA expression in the lungs of decompensated HF rats. Pulmonary IL-6 overexpression was associated with nuclear translocation of NF-{kappa}B and cytosolic degradation of I{kappa}B.

Conclusion: Dysfunctional pulmonary endothelium is a source of synthesis and storage of IL-6 in an experimental model of CHF.

Key Words: Myocardial infarction • Cytokines • Pulmonary circulation • Pulmonary edema • Heart failure

Received July 12, 2002; Revised October 23, 2002; Accepted December 12, 2002


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