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Cardiovascular Research 2003 60(1):141-146; doi:10.1016/S0008-6363(03)00362-6
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Enhanced expression of inflammatory cytokines and activation markers in T-cells from patients with chronic heart failure

Arne Yndestada,*, Are M Holma,b, Fredrik Müllera, Svein Simonsenc, Stig S Frølanda,b, Lars Gullestadd and Pål Aukrusta,b

aResearch Institute for Internal Medicine, Rikshospitalet, University of Oslo, N-0027 Oslo, Norway
bSection of Clinical Immunology and Infectious Diseases, Rikshospitalet, University of Oslo, N-0027 Oslo, Norway
cDepartment of Cardiology, Rikshospitalet, University of Oslo, Oslo, Norway
dMedical Department, Bærum Hospital, Sandvika, Norway

*Corresponding author. Tel.: +47-23-073-629; fax: +47-23-073-630. Email address: arne.yndestad{at}klinmed.uio.no

Objective: Increasing evidence supports a role for inflammation in chronic heart failure (CHF). However, the source and the mechanism for this immune activation are unknown. To address this issue we investigated the gene expression of cytokines and the surface expression of activity markers in T-cells and monocytes from CHF patients and healthy controls. Methods: Gene expression of cytokines was analysed by real-time RT-PCR and activation markers by flow cytometry in 14 CHF patients and nine healthy controls. Surface expression of activation markers for T-cells and monocytes were analysed by flow cytometry. Results: T-cells from CHF patients showed enhanced gene expression of chemokines, ligands in the tumor necrosis factor superfamily, as well as the inflammatory cytokines interferon-{gamma} and interleukin-18 with similar pattern in ischemic (n = 5) and idiopathic cardiomyopathy (n = 9). In contrast, no differences in cytokine gene expression were found comparing monocytes from CHF patients and controls. Moreover, T-cells from CHF patients had enhanced surface expression of the activation markers CD69 and CD25, while there was no upregulation of the monocyte activation marker CD32 in these patients. Conclusion: T-cells may be a part of the inflammatory response during CHF independent of the etiology of the disorder. Intervention preventing unwanted T-cell activation could represent a new target in the treatment of CHF.

KEYWORDS Heart failure; Immunology; Cytokines; Leukocytes; Gene expression

Time for primary review 22 days.


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