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?

Abstract

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.

• Authors: 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
• Journal: Mediators of inflammation (Mediators Inflamm) Vol. 2013 Pg. 498703 ( 2013) ISSN: 1466-1861 [Electronic] United States
• PMID: 24385685 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cytokines
• IL1RL1 protein, human
• IL33 protein, human
• Inflammation Mediators
• Interleukin-1 Receptor-Like 1 Protein
• Interleukin-33
• Interleukins
• Receptors, Cell Surface

Topics

• Cytokines (physiology)
• Female
• Heart Failure (etiology, immunology, therapy)
• Heart Transplantation
• Heart-Assist Devices
• Humans
• Inflammation Mediators (physiology)
• Interleukin-1 Receptor-Like 1 Protein
• Interleukin-33
• Interleukins (physiology)
• Male
• Middle Aged
• Receptors, Cell Surface (physiology)
• Signal Transduction