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The Immunoregulatory Role of Cytokines in Congestive Heart Failure | OMICS International | Abstract
ISSN: 2381-8727

International Journal of Inflammation, Cancer and Integrative Therapy
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Research Article

The Immunoregulatory Role of Cytokines in Congestive Heart Failure

Chen O1*, Patel J2, Mohamed E1, Greene M1, Moskovits N1and Shani J1

1Department of Cardiology, Maimonides Medical Center, Brooklyn, New York, USA

2Department of Internal Medicine, Maimonides Medical Center, Brooklyn, New York, USA

*Corresponding Author:
On Chen
Maimonides Medical Center
Department of Cardiology
Brooklyn, New York, USA
Tel: 631-2910908
Fax: 718-6357436
E-mail: [email protected]

Received date: August 14, 2014; Accepted date: September 23, 2014; Published date: September 25, 2014

Citation: Chen O, Patel J, Mohamed E, Greene M, Moskovits N, et al. (2014) The Immunoregulatory Role of Cytokines in Congestive Heart Failure. Microinflammation 1:111. doi: 10.4172/2381-8727.1000111

Copyright: © 2014 Chen O, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Cytokines have been shown to be associated with heart failure and to have multiple biological effects that can lead to left ventricular dysfunction, pulmonaryedema, and left ventricular remodeling. However, the effects of different cytokines, separately and in combination have not been fully determined. We aim to evaluate the levels of both pro-inflammatory and anti-inflammatory cytokines in patients with congestive heart failure (CHF), as well as in patients with coronary artery disease (CAD) and compare them to levels in normal controls (individuals without CHF or CAD) as to suggest their possible etiologic role.

Methods and results: In our study, the serum levels of IL-6, IL-10, IL-1β, IL-2 and TNF-α were measured in 19 patients with CHF, 18 patients with CAD without CHF and 8 controls, using immunoassays. There was a significant increase in the serum levels of IL-6, IL1-β, IL-10 and TNFα in the CHF group, and of IL-6, IL-1β and TNFα in the CAD group, compared with controls. Patients with CHF had significantly higher levels of anti-inflammatory cytokines IL-6 and IL-10 and lower levels of pro-inflammatory cytokines IL-2 compared when compared patients with CAD, emphasizing the different pathophysiologic mechanisms for these conditions.

Conclusion: Our studies suggest that patients with CHF had higher levels of Th2-type cytokines than patients with CAD, suggesting their role in the development of heart failure. Further studies are required to elucidate the role of cytokines in heart failure, and to understand the biological effects of cytokines and their role in the development of CHF. This may lead to development of new treatments modalities targeting their effects.

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