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Stress and Inflammation in Coronary Artery Disease: A Review Psychoneuroendocrineimmunology-Based

Fioranelli, Massimo, Bottaccioli, Anna G., Bottaccioli, Francesco, Bianchi, Maria, Rovesti, Miriam, Roccia, Maria G.·2018·Frontiers in Immunology
DOI 10.3389/fimmu.2018.02031PMC PMC6135895
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Figure 1 Pathological conditions that include common cardiovascular risk factors (such as hypertension, hyperlipidaemia, hyperglycaemia, smoking) and stress-related conditions (i.e. depression, anxiety) can elicit immune responses that promote the secretion of leukocyte adhesion molecules and chemotactic factors, inducing monocyte adhesion to endothelial cells and transmigration into the subintimal space. Initial atherosclerotic lesions begin with the differentiation of monocytes into macrophages that engulf cholesterol-rich oxidized lipoproteins to become foam cells that organize into fatty streaks. The perpetuation of pro-inflammatory and oxidizing atherosclerotic stimuli results in the recruitment of further macrophages, mast cells, and activated T and B cells that increase vascular lesions, which, in turn, releasing cytokines (i.e., IL-1β, TNF-α), increases monocytes migration into the subintimal space (17, 18, 19, 20). ICAM-1, Intercellular Adhesion Molecule 1; VCAM-1, Vascular cell adhesion protein 1; NLRP3, nucleotide-binding domain and leucine-rich repeat containing (NLR) family member pyrin domain-containing protein 3; IL-1β, Interleukin 1 beta; IL-6, Interleukin 6.
Figure 1 Pathological conditions that include common cardiovascular risk factors (such as hypertension, hyperlipidaemia, hyperglycaemia, smoking) and stress-related conditions (i.e. depression, anxiety) can elicit immune responses that promote the secretion of leukocyte adhesion molecules and chemotactic factors, inducing monocyte adhesion to endothelial cells and transmigration into the subintimal space. Initial atherosclerotic lesions begin with the differentiation of monocytes into macrophages that engulf cholesterol-rich oxidized lipoproteins to become foam cells that organize into fatty streaks. The perpetuation of pro-inflammatory and oxidizing atherosclerotic stimuli results in the recruitment of further macrophages, mast cells, and activated T and B cells that increase vascular lesions, which, in turn, releasing cytokines (i.e., IL-1β, TNF-α), increases monocytes migration into the subintimal space (17, 18, 19, 20). ICAM-1, Intercellular Adhesion Molecule 1; VCAM-1, Vascular cell adhesion protein 1; NLRP3, nucleotide-binding domain and leucine-rich repeat containing (NLR) family member pyrin domain-containing protein 3; IL-1β, Interleukin 1 beta; IL-6, Interleukin 6.CC BY · PubMed Central
Figure 2 Following myocardial infarction, cellular fragments released by dying or injured myocardial cells can trigger resident cardiac immune cells as endogenous “alarmins,” similar to microbial pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), through the engagement of membrane toll-like receptors (TLRs). Endogenous DAMPs can also activate the complement system, as observed with increased C3, C5 fragments in infarcted myocardial tissue, promoting leukocyte translocation in injured myocardium. Immune activation by DAMPs can arise also from mitochondrial DNA released by the mitochondria of damaged cardiac cells due to haemodynamic stress, inducing cardiomyocyte apoptosis. The generation of a large amount of reactive oxygen species (ROS) from mitochondria impairs myocardial function and activates leukocyte migration, reducing the number of vital cardiomyocytes and promoting extracellular matrix degradation. Many mediators of different origins can activate mast cells (MC) degranulation. In the first 24 h after an acute ischaemic cardiac event, endogenous DAMPs induce the release of histamine, TNF-α, IL-6, prostaglandins, leukotrienes, tryptase, chymase and renin from MCs, leading to an acute immune response, which, in turn, actives resident immune cells, like macrophages, T, B, and dendritic cells. DAMPs, damage-associated molecular patterns; ROS, reactive oxygen species; C5α, complement component 5 alfa; C3, complement component 3; TNF, tumor necrosis factor; IL-1/IL-1β, Interleukin 1/Interleukin 1 beta; TLR, toll-like receptor; IL-6, Interleukin 6.
Figure 2 Following myocardial infarction, cellular fragments released by dying or injured myocardial cells can trigger resident cardiac immune cells as endogenous “alarmins,” similar to microbial pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), through the engagement of membrane toll-like receptors (TLRs). Endogenous DAMPs can also activate the complement system, as observed with increased C3, C5 fragments in infarcted myocardial tissue, promoting leukocyte translocation in injured myocardium. Immune activation by DAMPs can arise also from mitochondrial DNA released by the mitochondria of damaged cardiac cells due to haemodynamic stress, inducing cardiomyocyte apoptosis. The generation of a large amount of reactive oxygen species (ROS) from mitochondria impairs myocardial function and activates leukocyte migration, reducing the number of vital cardiomyocytes and promoting extracellular matrix degradation. Many mediators of different origins can activate mast cells (MC) degranulation. In the first 24 h after an acute ischaemic cardiac event, endogenous DAMPs induce the release of histamine, TNF-α, IL-6, prostaglandins, leukotrienes, tryptase, chymase and renin from MCs, leading to an acute immune response, which, in turn, actives resident immune cells, like macrophages, T, B, and dendritic cells. DAMPs, damage-associated molecular patterns; ROS, reactive oxygen species; C5α, complement component 5 alfa; C3, complement component 3; TNF, tumor necrosis factor; IL-1/IL-1β, Interleukin 1/Interleukin 1 beta; TLR, toll-like receptor; IL-6, Interleukin 6.CC BY · PubMed Central
Graphical Abstract The current view of coronary heart disease has deeply changed: atherosclerosis is no longer considered a simple lipid storage disorder but a systemic inflammatory disease. Recent findings have fundamentally altered the classical vision of the heart as a “mechanical blood pump” that beats through an internal pacemaker. Indeed, cardiac tissue contains resident immune cells and is able to synthesize and release cytokines and hormones after acute myocardial infarction in the ischaemic area, influencing the healing phase. In recent years, chronic depression has ranked among the most important cardiovascular risk factors for poor prognosis in patients with myocardial infarction. Current understanding of the central and autonomic regulation of cardiac functions, namely, the neuro-cardiac axis, provides a physiological explanation that links psycho-emotional stressors and social adversities to acute cardiac event. Psychological distress can precipitate heart function through a dysregulated neuroendocrine and autonomic response. The complex network that links the heart, brain and the main biological systems provides a new vision of cardiovascular science based on psychoneuroendocrineimmunology, a science that studies the reciprocal interconnections between the psyche and nervous, immune and endocrine systems, integrating knowledge derived from the psychological and biological sciences of stress with molecular biology and epigenetic research. ACC, anterior cingulate cortex; HPA, hypothalamic–pituitary–adrenal axis; HRV, heart rate variability; ILs, interleukins; BP, blood pressure.
Graphical Abstract The current view of coronary heart disease has deeply changed: atherosclerosis is no longer considered a simple lipid storage disorder but a systemic inflammatory disease. Recent findings have fundamentally altered the classical vision of the heart as a “mechanical blood pump” that beats through an internal pacemaker. Indeed, cardiac tissue contains resident immune cells and is able to synthesize and release cytokines and hormones after acute myocardial infarction in the ischaemic area, influencing the healing phase. In recent years, chronic depression has ranked among the most important cardiovascular risk factors for poor prognosis in patients with myocardial infarction. Current understanding of the central and autonomic regulation of cardiac functions, namely, the neuro-cardiac axis, provides a physiological explanation that links psycho-emotional stressors and social adversities to acute cardiac event. Psychological distress can precipitate heart function through a dysregulated neuroendocrine and autonomic response. The complex network that links the heart, brain and the main biological systems provides a new vision of cardiovascular science based on psychoneuroendocrineimmunology, a science that studies the reciprocal interconnections between the psyche and nervous, immune and endocrine systems, integrating knowledge derived from the psychological and biological sciences of stress with molecular biology and epigenetic research. ACC, anterior cingulate cortex; HPA, hypothalamic–pituitary–adrenal axis; HRV, heart rate variability; ILs, interleukins; BP, blood pressure.CC BY · PubMed Central

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Authors
Fioranelli, M., Bottaccioli, A. G., Bottaccioli, F., Bianchi, M., Rovesti, M., & Roccia, M. G.
Venue
Frontiers in Immunology
Publisher
Frontiers Media SA
Published
2018-09-06
Volume
9
ISSN
1664-3224
DOI
10.3389/fimmu.2018.02031
PMC
PMC6135895
Cited by
302
References
27
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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