Next Article in Journal
1,2,4-Oxadiazole/2-Imidazoline Hybrids: Multi-target-directed Compounds for the Treatment of Infectious Diseases and Cancer
Next Article in Special Issue
Superantigenic Activation of Human Cardiac Mast Cells
Previous Article in Journal
Synthetic miR-143 Inhibits Growth of HER2-Positive Gastric Cancer Cells by Suppressing KRAS Networks Including DDX6 RNA Helicase
Previous Article in Special Issue
NFkappaB is a Key Player in the Crosstalk between Inflammation and Cardiovascular Diseases
Article Menu
Issue 7 (April-1) cover image

Export Article

Open AccessReview

Cross-Talk between Neurohormonal Pathways and the Immune System in Heart Failure: A Review of the Literature

1
Department of Medicine, Surgery and Odontology, University of Salerno, via S.Allende 1, 84081 Baronissi (SA), Italy
2
Department of Pharmacy, University of Salerno, via Giovanni Paolo II 132, 84084 Fisciano (SA), Italy
3
Casa di Cura Montevergine, 83013 Mercogliano (AV), Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(7), 1698; https://doi.org/10.3390/ijms20071698
Received: 12 March 2019 / Revised: 1 April 2019 / Accepted: 2 April 2019 / Published: 5 April 2019
(This article belongs to the Special Issue Mechanisms of Inflammation in Degenerative Cardiovascular Conditions)
  |  
PDF [2168 KB, uploaded 5 April 2019]
  |     |  

Abstract

Heart failure is a complex clinical syndrome involving a multitude of neurohormonal pathways including the renin-angiotensin-aldosterone system, sympathetic nervous system, and natriuretic peptides system. It is now emerging that neurohumoral mechanisms activated during heart failure, with both preserved and reduced ejection fraction, modulate cells of the immune system. Indeed, these cells express angiotensin I receptors, adrenoceptors, and natriuretic peptides receptors. Ang II modulates macrophage polarization, promoting M2 macrophages phenotype, and this stimulation can influence lymphocytes Th1/Th2 balance. β-AR activation in monocytes is responsible for inhibition of free oxygen radicals production, and together with α2-AR can modulate TNF-α receptor expression and TNF-α release. In dendritic cells, activation of β2-AR inhibits IL-12 production, resulting in the inhibition of Th1 and promotion of Th2 differentiation. ANP induces the activation of secretion of superoxide anion in polymorphonucleated cells; reduces TNF-α and nitric oxide secretion in macrophages; and attenuates the exacerbated TH1 responses. BNP in macrophages can stimulate ROS production, up-regulates IL-10, and inhibits IL-12 and TNF-α release by dendritic cells, suggesting an anti-inflammatory cytokines profile induction. Therefore, different neurohormonal-immune cross-talks can determine the phenotype of cardiac remodeling, promoting either favorable or maladaptive responses. This review aims to summarize the available knowledge on neurohormonal modulation of immune responses, providing supportive rational background for further research. View Full-Text
Keywords: heart failure; immune system; adrenergic system; renin-angiotensin-aldosterone system; natriuretic peptides system; neuro-immunomodulation; heart failure with preserved ejection fraction heart failure; immune system; adrenergic system; renin-angiotensin-aldosterone system; natriuretic peptides system; neuro-immunomodulation; heart failure with preserved ejection fraction
Figures

Figure 1

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 (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

De Angelis, E.; Pecoraro, M.; Rusciano, M.R.; Ciccarelli, M.; Popolo, A. Cross-Talk between Neurohormonal Pathways and the Immune System in Heart Failure: A Review of the Literature. Int. J. Mol. Sci. 2019, 20, 1698.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top