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European Journal of Heart Failure 2008 10(4):352-359; doi:10.1016/j.ejheart.2008.02.010
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© 2008 European Society of Cardiology

Increased expression of LIGHT/TNFSF14 and its receptors in experimental and clinical heart failure

Christen Peder Dahla,b,*, Lars Gullestadb, Børre Fevanga, Are M. Holmc, Linn Landrøa, Leif Erik Vinged, Arnt E. Fianee, Wiggo J. Sandberga, Kari Otterdala, Stig S. Frølanda,f, Jan Kristian Damåsa,f, Bente Halvorsena, Pål Aukrusta,f, Erik Øiea,b,d and Arne Yndestada

a Research Institute for Internal Medicine, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway
b Department of Cardiology, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway
c Department of Respiratory Medicine, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway
d Institute for Surgical Research, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway
e Department of Thoracic and Cardiovascular Surgery, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway
f Section of Clinical Immunology and Infectious Diseases, Rikshospitalet-Radiumhospitalet Medical Centre, University of Oslo Norway

* Corresponding author. Research Institute for Internal Medicine, Rikshospitalet-Radiumhospitalet Medical Centre, N-0027 Oslo, Norway. Tel.: +47 23072786; fax: +47 23073630. E-mail address: c.p.dahl{at}medisin.uio.no (C.P. Dahl).


  Abstract

Background: Clinical and experimental studies suggest a pathogenic role for inflammation in chronic heart failure (HF). LIGHT is a member of the tumour necrosis factor superfamily involved in innate and adaptive immune responses.

Aims: We sought to investigate a potential pathogenic role of LIGHT in chronic HF.

Methods: We used various clinical and experimental approaches including studies in post-infarction HF rats and in vitro studies of endothelial cells and peripheral blood mononuclear cells (PBMC).

Results: Our main findings were: (i) LIGHT and its receptors (i.e., HVEM and lymphotoxin-β receptor) were regulated during experimental HF, with strong expression in the infarcted area accompanied by up-regulation of HVEM in cardiomyocytes and endothelial cells also in the non-ischaemic part of the left ventricle. (ii) Patients with chronic HF had significantly increased expression of LIGHT on CD3+ T-cells accompanied by increased expression of HVEM on monocytes and within the failing myocardium. (iii) LIGHT induced interleukin (IL)-6 expression in endothelial cells. In HF patients, but not in healthy controls, such an IL-6-inducing effect was also seen in LIGHT activated PBMC.

Conclusion: Our findings in both clinical and experimental HF may suggest a role for LIGHT signalling pathways in the progression of chronic HF involving IL-6-related mechanisms.

Key Words: Heart failure • Inflammation • Cytokines • Tumour necrosis factor superfamily • Leukocytes

Received August 27, 2007; Revised November 26, 2007; Accepted February 4, 2008


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