Hindawi Publishing Corporation Mediators of Inlammation Volume 2013, Article ID 498703, 9 pages http://dx.doi.org/10.1155/2013/498703 Research Article IL-33/ST2 Pathway and Classical Cytokines in End-Stage Heart Failure Patients Submitted to Left Ventricular Assist Device Support: A Paradoxic Role for Inflammatory Mediators? C. Caselli, 1 A. D’Amico, 2 R. Ragusa, 1 R. Caruso, 3 T. Prescimone, 1 M. Cabiati, 1 S. Nonini, 4 P. Marraccini, 1,3 S. Del Ry, 1 M. G. Trivella, 1 O. Parodi, 1,3 and D. Giannessi 1 1 Laboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, Italy 2 Institute of Life Sciences, Scuola Superiore Sant’Anna, 56100 Pisa, Italy 3 Cardiovascular Department, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Niguarda C` a Granda Hospital, 20162 Milan, Italy 4 Cardiotoracovascular Department, Niguarda C` a Granda Hospital, 20162 Milan, Italy Correspondence should be addressed to C. Caselli; chiara.caselli@ifc.cnr.it Received 27 September 2013; Accepted 13 November 2013 Academic Editor: Peter N. Pushparaj Copyright © 2013 C. Caselli et al. his 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. Background. Inlammation is a critical process contributing to heart failure (HF). We hypothesized that IL-33/ST2 pathway, a new mechanism regulated during cardiac stress, may be involved in the functional worsening of end-stage HF patients, candidates for let ventricular assist device (LVAD) implantation, and potentially responsible for their outcome. Methods. IL-33, ST2, and conventional cytokines (IL-6, IL-8, and TNF-) were determined in cardiac biopsies and plasma of 22 patients submitted to LVAD implantation (pre-LVAD) and compared with (1) control stable chronic HF patients on medical therapy at the moment of heart transplantation without prior circulatory support (HT); (2) patients supported by LVAD at the moment of LVAD weaning (post- LVAD). Results. Cardiac expression of ST2/IL-33 and cytokines was lower in the pre-LVAD than in the HT group. LVAD determined an increase of inlammatory mediators comparable to levels of the HT group. Only ST2 correlated with outcome indices ater LVAD implantation. Conclusions. IL-33/ST2 and traditional cytokines were involved in decline of cardiac function of ESHF patients as well as in hemodynamic recovery induced by LVAD. IL-33/ST2 pathway was also associated to severity of clinical course. hus, a better understanding of inlammation is the key to achieving more favorable outcome by new speciic therapies. 1. Introduction Inlammation has emerged as a critical biological process contributing to nearly all aspects of cardiovascular disease including heart failure (HF) [1]. Several studies have iden- tiied the importance of proinlammatory mediators (such as TNF-, IL-6, and IL-8) in the development and pro- gression of HF [2–4]. hese factors can induce pathological myocardial remodeling by promoting the recruitment of inlammatory cells or by producing maladaptive efects in the heart on let ventricle (LV) function, such as LV remodel- ing and endothelial function, thus facilitating hypertrophic growth and ibrosis [5]. he recognition of inlammation as a common, important, and treatable condition in chronic HF has contributed to intensiied research for an efective anti- inlammatory therapy. However, the approaches tested so far have been largely disappointing, due to either neutral indings or a worsening of HF. hese discouraging results have raised important considerations, including the relevance of looking for novel targets evolving from basic research [6]. Recently, a number of studies have used gene expression, array screening, cloning, and other techniques to identify new cardiokines and cardiokine networks that are regulated during cardiac stress [4]. With mouse genetic approaches, many of these newly identiied factors have been shown to have functional roles in pathological cardiac remodeling.