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Disease Markers
Volume 28, Issue 2, Pages 115-124
http://dx.doi.org/10.3233/DMA-2010-0691

CD14CD16 Monocyte Subset Levels in Heart Failure Patients

Chiara Barisione,1 Silvano Garibaldi,1 Giorgio Ghigliotti,1 Patrizia Fabbi,1 Paola Altieri,1 Maria Carla Casale,1 Paolo Spallarossa,1 Giovanni Bertero,1 Manrico Balbi,1 Luca Corsiglia,2 and Claudio Brunelli1

1Division of Cardiology, Department of Internal Medicine, Research Center of Cardiovascular Biology, University of Genova, V.le Benedetto XV, 6 16132 Genova, Italy
2Casa Di Cura Istituto Cardiovascolare Camogli (ISC), Camogli, Italy

Received 25 March 2010; Accepted 25 March 2010

Copyright © 2010 Hindawi Publishing Corporation. 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

Our aim was to define the distribution of monocyte subsets in a cohort of congestive heart failure (CHF) patients, to verify whether increased severity of CHF is linked to the expansion of specific monocyte subsets, and finally to investigate the relationship between monocyte subset relative frequencies, laboratory parameters of inflammation, and monocyte ACE expression.

Thirty consecutive CHF patients and 26 healthy control subjects were evaluated for peripheral blood monocyte expression of CD14, CD16 and CD143 (ACE) by flow-cytometry, and for endothelial-derived soluble CD146 levels by ELISA.

CD14++CD16+ frequency was significantly higher in CHF patients than in Controls (%, median value and IQ) (12.3, 8.7–14.8 vs 5.9, 4.7–6.9, p++CD16+ levels. Frequencies of CD14+CD16+ monocytes were significantly lower in CHF patients as compared to Controls, and negatively correlated with levels of soluble CD146 (r = −0.529; p 0.048).

In conclusion, monocytic CD14++CD16+ frequency and CD143 levels are increased and reflect disease status and progressive cardiac deterioration in CHF patients. The CD14+CD16+ subset is depleted in CHF and is linked to endothelial damage in this group of patients.

Although the question of whether differences in monocyte CD14CD16 expansion are causal or whether they represent a marker of HF progression which is potentially relevant for risk prediction remains unanswered, we believe that our data represent an important tool for exploring the role of selective inflammatory pathways in CHF progression.