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?
Background. Inflammation 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 left ventricular assist device (LVAD) impla...
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| Format: | Article |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/498703 |
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| author | C. Caselli A. D'Amico R. Ragusa R. Caruso T. Prescimone M. Cabiati S. Nonini P. Marraccini S. Del Ry M. G. Trivella O. Parodi D. Giannessi |
| author_facet | C. Caselli A. D'Amico R. Ragusa R. Caruso T. Prescimone M. Cabiati S. Nonini P. Marraccini S. Del Ry M. G. Trivella O. Parodi D. Giannessi |
| author_sort | C. Caselli |
| collection | DOAJ |
| description | Background. Inflammation 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 left ventricular assist device (LVAD) implantation, and potentially responsible for their outcome. Methods. IL-33, ST2, and conventional cytokines (IL-6, IL-8, and TNF-α) 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 inflammatory mediators comparable to levels of the HT group. Only ST2 correlated with outcome indices after 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. Thus, a better understanding of inflammation is the key to achieving more favorable outcome by new specific therapies. |
| format | Article |
| id | doaj-art-db1addff5dbe4bea870bf3ec42e3ab47 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-db1addff5dbe4bea870bf3ec42e3ab472025-08-20T03:24:26ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/498703498703IL-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. Caselli0A. D'Amico1R. Ragusa2R. Caruso3T. Prescimone4M. Cabiati5S. Nonini6P. Marraccini7S. Del Ry8M. G. Trivella9O. Parodi10D. Giannessi11Laboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyInstitute of Life Sciences, Scuola Superiore Sant’Anna, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyCardiovascular Department, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Niguarda Cà Granda Hospital, 20162 Milan, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyCardiotoracovascular Department, Niguarda Cà Granda Hospital, 20162 Milan, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyLaboratory of Cardiovascular Biochemistry, Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche (CNR), Area della Ricerca, Via Moruzzi 1, 56100 Pisa, ItalyBackground. Inflammation 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 left ventricular assist device (LVAD) implantation, and potentially responsible for their outcome. Methods. IL-33, ST2, and conventional cytokines (IL-6, IL-8, and TNF-α) 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 inflammatory mediators comparable to levels of the HT group. Only ST2 correlated with outcome indices after 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. Thus, a better understanding of inflammation is the key to achieving more favorable outcome by new specific therapies.http://dx.doi.org/10.1155/2013/498703 |
| spellingShingle | C. Caselli A. D'Amico R. Ragusa R. Caruso T. Prescimone M. Cabiati S. Nonini P. Marraccini S. Del Ry M. G. Trivella O. Parodi D. Giannessi 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? Mediators of Inflammation |
| title | 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? |
| title_full | 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? |
| title_fullStr | 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? |
| title_full_unstemmed | 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? |
| title_short | 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? |
| title_sort | 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 |
| url | http://dx.doi.org/10.1155/2013/498703 |
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