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Biomedicines
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Neuroinflammation in Stress-Related Disorders
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Neuroinflammation in Stress-Related Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 31538

Special Issue Editors

Dr. Marta Rodríguez-Arias

E-Mail Website
Guest Editor
Unit of Research Psychobiology of Drug Dependence, Department of Psychobiology, Facultad de Psicología, Universitat de Valencia, Avda. Blasco Ibáñez, 21, 46010 Valencia, Spain
Interests: drug abuse; animal models; social stress; diet; neuroinflammation; alcohol; cocaine
Dr. Carmen Ferrer-Perez

E-Mail Website
Guest Editor
Department of Psychology and Sociology, University of Zaragoza, C/Ciudad Escolar s/n, 44003 Teruel, Spain
Interests: neuroscience;animal models;neuroinflammation; drug addiction; social stress; conditioned place preference; CRF; IL-6; depression-like behavior

Special Issue Information

Dear Colleagues,

This Special Issue, “Neuroinflammation in Stress-Related Disorders”, will mainly focus on the immune and inflammatory mechanisms underlying stress-related disorders.

Stress response is a healthy and adaptive strategy that helps us to cope with acute challenges to our survival. In modern society, we live in a complex social environment with constantly demanding conditions that are inescapable parts of our daily routine and stress has become a significant problem. This exposure to persistent stressors may promote long-lasting adverse effects on our health, both in physiological and psychological dimensions. In fact, there is vast literature linking stress to some epidemic diseases in our society, such as cancer, obesity, anxiety, depression, neurodegenerative disease, and drug addiction among others. Consequently, there is growing interest in characterizing the mechanisms involved in the pathogenesis of different stress-related disorders. Recent basic research has pointed to a new neurobiological target: the immune system. In this regard, numerous studies have demonstrated that immune processes may not only be provoked by pathological conditions, but can also be triggered by stress.

We cordially invite authors to submit clinical and preclinical original research or review manuscripts focused on three different aspects: (a) the mechanism that links stress experiences and the induction of inflammation, including but not limited to the role of microbiota and the gut–brain axis, how peripheral inflammation turns into neuroinflammation, mediators of the inflammatory response (chemokines, cytokines, etc.), and molecular mechanisms of the activation of neuroimmune cells; (b) the consequences of stress-induced neuroinflammation in neurodegenerative and neurological impairment, cognitive impairment, depression and anxiety, and substance use disorders; (c) new therapeutic approaches in stress-related disorders that target the immune system as a novel approach in any of the steps between stress, inflammation, and its consequences.

Dr. Marta Rodríguez-Arias
Dr. Carmen Ferrer-Perez
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neuroinflammation
  • stress-related disorders
  • drug addiction
  • depression
  • neurodegenerative disease
  • animal models
  • clinical studies
  • resilience
  • drug addiction
  • generalized anxiety disorder
  • gut microbiome
  • dysbiosis
  • social phobia
  • obsessive-compulsive disorder

Published Papers (8 papers)

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Research

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23 pages, 3674 KiB  
Article
Effect of Voluntary Wheel-Running Exercise on the Endocrine and Inflammatory Response to Social Stress: Conditioned Rewarding Effects of Cocaine
by Carmen Ferrer-Pérez, Marina D. Reguilón, José Miñarro and Marta Rodríguez-Arias
Biomedicines 2022, 10(10), 2373; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10102373 - 23 Sep 2022
Cited by 3 | Viewed by 1771
Abstract
The present paper evaluates the effect of physical activity on the increase of the conditioned rewarding effects of cocaine induced by intermittent social stress and on the neuroinflammatory response that contributes to the enhancement of drug response. For that purpose, three studies were [...] Read more.
The present paper evaluates the effect of physical activity on the increase of the conditioned rewarding effects of cocaine induced by intermittent social stress and on the neuroinflammatory response that contributes to the enhancement of drug response. For that purpose, three studies were designed in which social stress was induced in different samples of mice through a social-defeat protocol; the mice underwent an increase of physical activity by different modalities of voluntary wheel running (continuous and intermittent access). The results showed that continuous access to running wheels prior to stress enhanced the establishment of cocaine place preference, whereas an intermittent access exerted a protective effect. Wheel running contingent to cocaine administration prevented the development of conditioned preference, and if applied during the extinction of drug memories, it exerted a dual effect depending on the stress background of the animal. Our biological analysis revealed that increased sensitivity to cocaine may be related to the fact that wheel running promotes inflammation though the increase of IL-6 and BDNF levels. Together, these results highlight that physical exercise deeply impacts the organism’s response to stress and cocaine, and these effects should be taken into consideration in the design of a physical intervention. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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16 pages, 2713 KiB  
Article
In Vivo Cerebral Translocator Protein (TSPO) Binding and Its Relationship with Blood Adiponectin Levels in Treatment-Naïve Young Adults with Major Depression: A [11C]PK11195 PET Study
by Yo-Han Joo, Min-Woo Lee, Young-Don Son, Keun-A Chang, Maqsood Yaqub, Hang-Keun Kim, Paul Cumming and Jong-Hoon Kim
Biomedicines 2022, 10(1), 34; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10010034 - 24 Dec 2021
Cited by 2 | Viewed by 2910
Abstract
Adiponectin is an adipokine that mediates cellular cholesterol efflux and plays important roles in neuroinflammatory processes. In this study, we undertook positron emission tomography (PET) with the translocator protein (TSPO) ligand [11C]PK11195 and measured serum adiponectin levels in groups of treatment-naïve [...] Read more.
Adiponectin is an adipokine that mediates cellular cholesterol efflux and plays important roles in neuroinflammatory processes. In this study, we undertook positron emission tomography (PET) with the translocator protein (TSPO) ligand [11C]PK11195 and measured serum adiponectin levels in groups of treatment-naïve young adult patients with major depressive disorder (MDD) and matched healthy controls. Thirty treatment-naïve MDD patients (median age: 24 years) and twenty-three healthy controls underwent [11C]PK11195 PET. We quantified TSPO availability in brain as the [11C]PK11195 binding potential (BPND) using a reference tissue model in conjunction with the supervised cluster analysis (SVCA4) algorithm. Age, sex distribution, body mass index, and serum adiponectin levels did not differ between the groups. Between-group analysis using a region-of-interest approach showed significantly higher [11C]PK11195 BPND in the left anterior and right posterior cingulate cortices in MDD patients than in controls. Serum adiponectin levels had significant negative correlations with [11C]PK11195 BPND in the bilateral hippocampus in MDD patients, but significant positive correlations in the bilateral hippocampus in the control group. Our results indicate significantly higher TSPO binding in the anterior and posterior cingulate cortices in treatment-naïve young MDD patients, suggesting microglial activation in these limbic regions, which are involved in cognitive and emotional processing. The opposite correlations between [11C]PK11195 BPND in the hippocampus with serum adiponectin levels in MDD and control groups suggest that microglial activation in the hippocampus may respond differentially to adiponectin signaling in MDD and healthy subjects, possibly with respect to microglial phenotype. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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13 pages, 1887 KiB  
Article
Sex Difference in Peripheral Inflammatory Biomarkers in Drug-Naïve Patients with Major Depression in Young Adulthood
by Jinho Kim, Jong-Hoon Kim and Keun-A Chang
Biomedicines 2021, 9(7), 708; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9070708 - 22 Jun 2021
Cited by 13 | Viewed by 2255
Abstract
The number of patients with major depressive disorder (MDD) is increasing worldwide. In particular, the early onset of MDD from adolescence to young adulthood is more problematic than the later onset. The specific and expeditious identification of MDD before the occurrence of severe [...] Read more.
The number of patients with major depressive disorder (MDD) is increasing worldwide. In particular, the early onset of MDD from adolescence to young adulthood is more problematic than the later onset. The specific and expeditious identification of MDD before the occurrence of severe symptoms is significant for future interventions or therapies; however, there is no accurate diagnostic marker that has sufficient sensitivity and specificity for clinical use. In the present study, to identify the possibility of blood markers for depression, we first measured the baseline inflammatory biomarkers in the peripheral blood of 50 treatment-naïve young adults with MDD and 50 matched healthy controls. We then analyzed the correlation between prospective biomarkers and depressive symptoms using scores from various clinical depression indices. We also identified differential responses between males and females in prospective biomarkers. In young adulthood, men with MDD had increased peripheral interleukin (IL)-17 levels, whereas women with MDD had significantly increased IL-1β, IL-6, and C-reactive protein (CRP) levels compared with healthy controls. However, tumor necrosis factor-α (TNF-α), CCL1, CCL2, adiponectin, and cortisol were not significantly different in young adult individuals with MDD. Higher levels of IL-17 in the male group and of IL-1β, IL-6, and CRP in the female group may have been associated with the clinical symptoms of MDD, including depressive moods, hopelessness, suicidal ideation, low self-esteem, and reduced psychological resilience. Our findings will be useful in developing diagnostic tools or treatments for MDD in young adulthood. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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Review

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14 pages, 1070 KiB  
Review
Pharmacological Treatment for Neuroinflammation in Stress-Related Disorder
by Dong-Hun Lee, Ji-Young Lee, Dong-Yong Hong, Eun-Chae Lee, Sang-Won Park, Yun-Kyung Lee and Jae-Sang Oh
Biomedicines 2022, 10(10), 2518; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10102518 - 09 Oct 2022
Cited by 4 | Viewed by 6843
Abstract
Stress is an organism’s response to a biological or psychological stressor, a method of responding to threats. The autonomic nervous system and hypothalamic–pituitary–adrenal axis (HPA axis) regulate adaptation to acute stress and secrete hormones and excitatory amino acids. This process can induce excessive [...] Read more.
Stress is an organism’s response to a biological or psychological stressor, a method of responding to threats. The autonomic nervous system and hypothalamic–pituitary–adrenal axis (HPA axis) regulate adaptation to acute stress and secrete hormones and excitatory amino acids. This process can induce excessive inflammatory reactions to the central nervous system (CNS) by HPA axis, glutamate, renin-angiotensin system (RAS) etc., under persistent stress conditions, resulting in neuroinflammation. Therefore, in order to treat stress-related neuroinflammation, the improvement effects of several mechanisms of receptor antagonist and pharmacological anti-inflammation treatment were studied. The N-methyl-D-aspartate (NMDA) receptor antagonist, peroxisome proliferator-activated receptor agonist, angiotensin-converting enzyme inhibitor etc., effectively improved neuroinflammation. The interesting fact is that not only can direct anti-inflammation treatment improve neuroinflammation, but so can stress reduction or pharmacological antidepressants. The antidepressant treatments, including selective serotonin reuptake inhibitors (SSRI), also helped improve stress-related neuroinflammation. It presents the direction of future development of stress-related neuroinflammation drugs. Therefore, in this review, the mechanism of stress-related neuroinflammation and pharmacological treatment candidates for it were reviewed. In addition, treatment candidates that have not yet been verified but indicate possibilities were also reviewed. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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14 pages, 658 KiB  
Review
The Relationship between Stress, Inflammation, and Depression
by Il-Bin Kim, Jae-Hon Lee and Seon-Cheol Park
Biomedicines 2022, 10(8), 1929; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10081929 - 09 Aug 2022
Cited by 24 | Viewed by 6310
Abstract
A narrative review about the relationship between stress, inflammation, and depression is made as follows: Chronic stress leads to various stress-related diseases such as depression. Although most human diseases are related to stress exposure, the common pathways between stress and pathophysiological processes of [...] Read more.
A narrative review about the relationship between stress, inflammation, and depression is made as follows: Chronic stress leads to various stress-related diseases such as depression. Although most human diseases are related to stress exposure, the common pathways between stress and pathophysiological processes of different disorders are still debatable. Chronic inflammation is a crucial component of chronic diseases, including depression. Both experimental and clinical studies have demonstrated that an increase in the levels of pro-inflammatory cytokines and stress hormones, such as glucocorticoids, substantially contributes to the behavioral alterations associated with depression. Evidence suggests that inflammation plays a key role in the pathology of stress-related diseases; however, this link has not yet been completely explored. In this study, we aimed to determine the role of inflammation in stress-induced diseases and whether a common pathway for depression exists. Recent studies support pharmacological and non-pharmacological treatment approaches significantly associated with ameliorating depression-related inflammation. In addition, major depression can be associated with an activated immune system, whereas antidepressants can exert immunomodulatory effects. Moreover, non-pharmacological treatments for major depression (i.e., exercise) may be mediated by anti-inflammatory actions. This narrative review highlights the mechanisms underlying inflammation and provides new insights into the prevention and treatment of stress-related diseases, particularly depression. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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17 pages, 2379 KiB  
Review
Neuroinflammation in Post-Traumatic Stress Disorder
by Dong-Hun Lee, Ji-Young Lee, Dong-Yong Hong, Eun-Chae Lee, Sang-Won Park, Man-Ryul Lee and Jae-Sang Oh
Biomedicines 2022, 10(5), 953; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10050953 - 20 Apr 2022
Cited by 17 | Viewed by 5495
Abstract
Post-traumatic stress disorder (PTSD) is a well-known mental illness, which is caused by various stressors, including memories of past physical assaults and psychological pressure. It is diagnosed as a mental and behavioral disorder, but increasing evidence is linking it to the immune system [...] Read more.
Post-traumatic stress disorder (PTSD) is a well-known mental illness, which is caused by various stressors, including memories of past physical assaults and psychological pressure. It is diagnosed as a mental and behavioral disorder, but increasing evidence is linking it to the immune system and inflammatory response. Studies on the relationship between inflammation and PTSD revealed that patients with PTSD had increased levels of inflammatory cytokine biomarkers, such as interleukin-1, interleukin-6, tumor necrosis factor-α, nuclear factor-κB, and C-reactive protein, compared with healthy controls. In addition, animal model experiments imitating PTSD patients suggested the role of inflammation in the pathogenesis and pathophysiology of PTSD. In this review, we summarize the definition of PTSD and its association with increased inflammation, its mechanisms, and future predictable diseases and treatment possibilities. We also discuss anti-inflammatory treatments to address inflammation in PTSD. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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9 pages, 532 KiB  
Review
Possible Association of Cholesterol as a Biomarker in Suicide Behavior
by Thelma Beatriz González-Castro, Alma Delia Genis-Mendoza, Dulce Ivannia León-Escalante, Yazmín Hernández-Díaz, Isela Esther Juárez-Rojop, Carlos Alfonso Tovilla-Zárate, María Lilia López-Narváez, Alejandro Marín-Medina, Humberto Nicolini, Rosa Giannina Castillo-Avila and Miguel Ángel Ramos-Méndez
Biomedicines 2021, 9(11), 1559; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9111559 - 28 Oct 2021
Cited by 4 | Viewed by 2115
Abstract
Suicides and suicidal behavior are major causes of mortality and morbidity in public health and are a global problem. Various authors have proposed changes in lipid metabolism (total cholesterol decrease) as a possible biological marker for suicidal behavior. The objective of this study [...] Read more.
Suicides and suicidal behavior are major causes of mortality and morbidity in public health and are a global problem. Various authors have proposed changes in lipid metabolism (total cholesterol decrease) as a possible biological marker for suicidal behavior. The objective of this study was to review the studies that have demonstrated a relationship between serum cholesterol levels and suicidal behavior and to describe the possible pathophysiological mechanisms that associate changes in cholesterol concentration and suicidal behavior. Relevant literature related to serum cholesterol levels and suicidal behavior was identified through various database searches. The data from the existing literature present the findings that relate low cholesterol levels and possible pathophysiological mechanisms (neuroinflammation, serotonergic neurotransmission), genes related to cholesterol synthesis, pharmacological treatments that alter lipid metabolism and the possible participation in suicidal behavior. Nevertheless, future research is required to describe how serum cholesterol affects cholesterol metabolism in the CNS to establish and understand the role of cholesterol in suicidal behavior. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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Other

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31 pages, 2739 KiB  
Systematic Review
Clinical Value of Inflammatory and Neurotrophic Biomarkers in Bipolar Disorder: A Systematic Review and Meta-Analysis
by Amanda Vega-Núñez, Carlos Gómez-Sánchez-Lafuente, Fermín Mayoral-Cleries, Antonio Bordallo, Fernando Rodríguez de Fonseca, Juan Suárez and José Guzmán-Parra
Biomedicines 2022, 10(6), 1368; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10061368 - 09 Jun 2022
Cited by 4 | Viewed by 2406
Abstract
Bipolar disorder (BD) is a multifactorial chronic psychiatric disease highly defined by genetic, clinical, environmental and social risk factors. The present systematic review and meta-analysis aimed to examine the relationship between inflammatory and neurotrophic factors and clinical, social and environmental factors involved in [...] Read more.
Bipolar disorder (BD) is a multifactorial chronic psychiatric disease highly defined by genetic, clinical, environmental and social risk factors. The present systematic review and meta-analysis aimed to examine the relationship between inflammatory and neurotrophic factors and clinical, social and environmental factors involved in the development and the characterization of BD. Web of Science, PubMed, PsycINFO, Scopus and Science Direct were searched by two independent reviewers. The systematic review was registered in PROSPERO (CRD42020180626). A total of 51 studies with 4547 patients with a diagnosis of BD were selected for systematic review. Among them, 18 articles were included for meta-analysis. The study found some evidence of associations between BDNF and/or inflammatory factors and different stressors and functional and cognitive impairment, but limitations prevented firm conclusions. The main finding of the meta-analysis was a negative correlation between circulating levels of BDNF and depression severity score (standardized mean difference = −0.22, Confidence Interval 95% = −0.38, −0.05, p = 0.01). Evidence indicates that BDNF has a role in the depressive component of BD. However, the poor consistency found for other inflammatory mediators clearly indicates that highly controlled studies are needed to identity precise biomarkers of this disorder. Full article
(This article belongs to the Special Issue Neuroinflammation in Stress-Related Disorders)
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