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Mediators of Inflammation
Volume 2012 (2012), Article ID 616384, 9 pages
http://dx.doi.org/10.1155/2012/616384
Research Article

Changes in the Monocytic Subsets CD14dimCD16+ and CD14++CD16 in Chronic Systolic Heart Failure Patients

1Heart Failure Center, Division of Cardiology, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel
2Immunology Research Unit, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel
3Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel

Received 22 August 2012; Revised 11 October 2012; Accepted 25 October 2012

Academic Editor: Chiou-Feng Lin

Copyright © 2012 Offer Amir et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Different monocytic subsets are important in inflammation and tissue remodelling, but although heart failure (HF) is associated with local and systemic inflammation, their roles in HF are yet unknown. We recruited 59 chronic systolic HF patients (aged years, 45 males and 14 females) and 29 age-matched controls with no pervious heart disease. Compared to the controls, we found no change in the distribution of the CD14+CD16+ monocytic subset, whereas the classical CD14++CD16 subset was decreased by 11% ( ), and the nonclassical CD14dimCD16+ subset was expanded by 4% ( ) in HF patients and was inversely associated with severe HF ( ), as assessed by increased end-diastolic dimension (EDD). Compared to the control group, serum TNF , IL-1 , IL-10, and IL-13 levels were significantly elevated in the HF patients. Specifically, IL-13 levels were positively correlated to the CD1CD14dimCD16+ monocytic subset ( , ), and intracellular staining of IL-13 demonstrated that some of these monocytes produce the cytokine in HF patients, but not in the controls. We suggest that the inverse association between EDD values and the expansion of CD1 CD16+ monocytes that can produce IL-13 could be explained as a measure to counterbalance adverse remodelling, which is a central process in HF.