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Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment
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Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment

A special issue of Pharmaceuticals (ISSN 1424-8247).

Deadline for manuscript submissions: closed (30 November 2018) | Viewed by 74188

Special Issue Editors

Prof. Dr. S. Mechiel Korte

E-Mail Website
Guest Editor
Department of Biopsychology, Faculty of Psychology, Ruhr-Universität Bochum, Universitätsstraße 150, D-44780 Bochum, Germany
Interests: inflammation; fatigue; depression; sickness behavior; neuroimmunology; brain mechanisms; human wellbeing; animal welfare; quality of life
Dr. Jan-Pieter Konsman

E-Mail Website
Guest Editor
CNRS UMR 5287 Institute for Cognitive and Integrative Neurosciences in Aquitaine (INCIA), University of Bordeaux, 33076 Bordeaux, France
Interests: blood-brain interface; cytokine; food intake; inflammation; sickness behavior
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The focus of this Special Issue is on research that aims to understand the neuroimmune mechanisms that influence psychiatric disorders. Coming from studying of seemingly different fields of research, i.e., immunology, endocrinology, neuroscience, and pharmacology, elements that were previously considered to be domains of one discipline are now discovered in the other.

This Special Issue may include manuscripts on the role of immune system in triggering inflammation in the body and brain that affects regulatory circuits involved in emotion, motivation, and cognition. We hope that this Special Issue will clarify our understanding of the neuroimmune mechanisms that underlie the changes in activity in neural circuits controlling physiology and behavior, with important implications for public health with respect to stress, fatigue, anxiety, depression etc. This Special Issue is of particular importance because understanding these neuroimmune mechanisms could lead to novel therapeutic targets for mental illnesses.

In this Special Issue, we would like to cover the most recent neuroimmune correlates involved in brain pathology. Very welcome are studies proving a link between inflammation and clinical features such as chemistry, brain signals, neuro- and psychopathology, emotional and cognitive dysfunction.

We welcome original research, reviews, case reports, clinical trials, hypothesis and theory, methods, and perspectives, from international researchers and clinicians in this field. The purpose of this Special Issue is intended to provide the field with current approaches in psychoneuroimmunology and neuroimmunopharmacology that is hoped to improve and create therapeutic options for inflammation-related brain disorders.

Prof. Dr. S. Mechiel Korte
Dr. Jan-Pieter Konsman
Guest Editor

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. Pharmaceuticals 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 2900 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

  • Inflammation
  • Mental Disorders
  • Immunology
  • Neuroscience
  • Pharmacology
  • Brain Mechanisms
  • Behavior
  • Psychiatry
  • Psychology

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Published Papers (7 papers)

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Research

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17 pages, 2109 KiB  
Article
Juvenile Arthritis Patients Suffering from Chronic Inflammation Have Increased Activity of Both IDO and GTP-CH1 Pathways But Decreased BH4 Efficacy: Implications for Well-Being, Including Fatigue, Cognitive Impairment, Anxiety, and Depression
by Gerdien A. H. Korte-Bouws, Eline Albers, Marije Voskamp, Hendrikus Hendriksen, Lidewij R. De Leeuw, Onur Güntürkün, Sytze De Roock, Sebastiaan J. Vastert and S. Mechiel Korte
Pharmaceuticals 2019, 12(1), 9; https://doi.org/10.3390/ph12010009 - 8 Jan 2019
Cited by 24 | Viewed by 6362
Abstract
Juvenile idiopathic arthritis (JIA) represents joint inflammation with an unknown cause that starts before the age of 16, resulting in stiff and painful joints. In addition, JIA patients often report symptoms of sickness behavior. Recent animal studies suggest that proinflammatory cytokines produce sickness [...] Read more.
Juvenile idiopathic arthritis (JIA) represents joint inflammation with an unknown cause that starts before the age of 16, resulting in stiff and painful joints. In addition, JIA patients often report symptoms of sickness behavior. Recent animal studies suggest that proinflammatory cytokines produce sickness behavior by increasing the activity of indoleamine-2,3-dioxygenase (IDO) and guanosinetriphosphate–cyclohydrolase-1 (GTP–CH1). Here, it is hypothesized that inflammation in JIA patients enhances the enzymatic activity of IDO and GTP-CH1 and decreases the co-factor tetrahydrobiopterin (BH4). These compounds play a crucial role in the synthesis and metabolism of neurotransmitters. The aim of our study was to reveal whether inflammation affects both the GTP-CH1 and IDO pathway in JIA patients. Serum samples were collected from twenty-four JIA patients. In these samples, the concentrations of tryptophan (TRP), kynurenine (KYN), tyrosine (TYR), neopterin, and phenylalanine (PHE) were measured. An HPLC method with electrochemical detection was developed to quantify tryptophan, kynurenine, and tyrosine. Neopterin and phenylalanine were quantified by ELISA. The KYN/TRP ratio was measured as an index of IDO activity, while the PHE/TYR ratio was measured as an index of BH4 activity. Neopterin concentrations were used as an indirect measure of GTP-CH1 activity. JIA patients with high disease activity showed higher levels of both neopterin and kynurenine, and a higher ratio of both KYN/TRP and PHE/TYR and lower tryptophan levels than clinically inactive patients. Altogether, these data support our hypothesis that inflammation increases the enzymatic activity of both IDO and GTP-CH1 but decreases the efficacy of the co-factor BH4. In the future, animal studies are needed to investigate whether inflammation-induced changes in these enzymatic pathways and co-factor BH4 lower the levels of the brain neurotransmitters glutamate, noradrenaline, dopamine, serotonin, and melatonin, and consequently, whether they may affect fatigue, cognition, anxiety, and depression. Understanding of these complex neuroimmune interactions provides new possibilities for Pharma-Food interventions to improve the quality of life of patients suffering from chronic inflammation. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
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12 pages, 1918 KiB  
Article
Bacterial Lipopolysaccharide Increases Serotonin Metabolism in Both Medial Prefrontal Cortex and Nucleus Accumbens in Male Wild Type Rats, but Not in Serotonin Transporter Knockout Rats
by Gerdien A. H. Korte-Bouws, Floor Van Heesch, Koen G. C. Westphal, Lisa M. J. Ankersmit, Edwin M. Van Oosten, Onur Güntürkün and S. Mechiel Korte
Pharmaceuticals 2018, 11(3), 66; https://doi.org/10.3390/ph11030066 - 5 Jul 2018
Cited by 19 | Viewed by 5968
Abstract
It is well known that bacterial lipopolysaccharides (LPS) both increases proinflammatory cytokines and produces sickness behavior, including fatigue and anhedonia (i.e., the inability to experience pleasure). Previously, we have shown that intraperitoneally (i.p.) administered LPS increased extracellular monoamine metabolite levels in the nucleus [...] Read more.
It is well known that bacterial lipopolysaccharides (LPS) both increases proinflammatory cytokines and produces sickness behavior, including fatigue and anhedonia (i.e., the inability to experience pleasure). Previously, we have shown that intraperitoneally (i.p.) administered LPS increased extracellular monoamine metabolite levels in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), which was completely, or at least partly, prevented by pretreatment with a triple reuptake inhibitor that also blocks the serotonin (5-HT) transporter (SERT). This suggests indirectly, that LPS may enhance SERT transporter activity, and consequently, increase removal of 5-HT from the synaptic cleft, and increase metabolism of 5-HT. In the present study, we focus more specifically on the role of SERT in this increased metabolism by using rats, that differ in SERT expression. Therefore, the effects of an intraperitoneal LPS injection on extracellular concentrations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) were investigated by in vivo microdialysis in the NAc and mPFC of wild type (SERT+/+), heterozygous (SERT+/−) and knockout (SERT−/−) rats. Here, we show that LPS-induced 5-HIAA formation in male rats, is significantly increased in SERT+/+ rats in both the NAc and mPFC, whereas this increase is partly or totally abolished in SERT+/− and SERT−/− rats, respectively. Thus, the present study supports the hypothesis that systemic LPS in male rats increases SERT function and consequently enhances 5-HT uptake and metabolism in both the NAc and mPFC. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
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Review

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18 pages, 347 KiB  
Review
Inflammation and Depression: A Nervous Plea for Psychiatry to Not Become Immune to Interpretation
by Jan Pieter Konsman
Pharmaceuticals 2019, 12(1), 29; https://doi.org/10.3390/ph12010029 - 14 Feb 2019
Cited by 21 | Viewed by 5472
Abstract
The possibility that inflammation plays a causal role in major depression is an important claim in the emerging field of immunopsychiatry and has generated hope for new treatments. The aims of the present review are first to provide some historical background and to [...] Read more.
The possibility that inflammation plays a causal role in major depression is an important claim in the emerging field of immunopsychiatry and has generated hope for new treatments. The aims of the present review are first to provide some historical background and to consider the evidence in favor of the claim that inflammation is causally involved in major depression. The second part discusses some of the possibilities allowed for by the use of broad ‘umbrella’ concepts, such as inflammation and stress, in terms of proposing new working hypotheses and potential mechanisms. The third part reviews proposed biomarkers of inflammation and depression and the final part addresses how elements discussed in the preceding sections are used in immunopsychiatry. The ‘umbrella’ concepts of inflammation and stress, as well as insufficiently-met criteria based inferences and reverse inferences are being used to some extent in immunopsychiatry. The field is therefore encouraged to specify concepts and constructs, as well as to consider potential alternative interpretations and explanations for findings obtained. The hope is that pointing out some of the potential problems will allow for a clearer picture of immunopsychiatry’s current strengths and limitations and help the field mature. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
17 pages, 892 KiB  
Review
Insights into Macrophage Heterogeneity and Cytokine-Induced Neuroinflammation in Major Depressive Disorder
by Adwitia Dey and Pamela A. Hankey Giblin
Pharmaceuticals 2018, 11(3), 64; https://doi.org/10.3390/ph11030064 - 25 Jun 2018
Cited by 54 | Viewed by 8458
Abstract
Over 350 million individuals suffer from depression, a psychiatric illness classified as major depressive disorder (MDD) with symptoms that include a loss of interest or pleasure in life accompanied by depressed mood. The present understanding of major depressive disorder does not encompass a [...] Read more.
Over 350 million individuals suffer from depression, a psychiatric illness classified as major depressive disorder (MDD) with symptoms that include a loss of interest or pleasure in life accompanied by depressed mood. The present understanding of major depressive disorder does not encompass a systematic characterization of the neurobiological processes that drive the behavioral physiology in patients diagnosed with major depressive disorder. Psychiatric illness is a complex intersection between genetics, physiology, immunology and environmental stress. The increased attention to the relevance of depression has led to new discoveries that highlight the biological significance of ‘neuroinflammation’ and immunity underlying a spectrum of psychiatric illnesses. The process of neuroinflammation involves sentinel immune cells in the central nervous system (CNS). The activation and polarization of microglia, CNS-resident macrophages, modulates the production and secretion of pro-inflammatory cytokines implicated in the etiology of major depressive disorder, and this phenomenon has been aptly titled the ‘macrophage theory of depression’. Of particular interest are three hallmark cytokines, IL-6, TNFα and IL-1β, which have been studied extensively in basic research, cell-receptor signaling and drug development. The field of inflammasome-mediated neuroinflammation is an emerging area of MDD research that is providing new cellular insight into how macrophages mechanistically support cytokine-associated neuropathology, particularly in the case of IL-1β-associated inflammation in MDD. With the increasing number of individuals identified with depression, a comprehensive understanding of macrophage-cytokine signaling pathways in the CNS in depression is necessary for developing effective anti-depressant therapeutics. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
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17 pages, 913 KiB  
Review
Role of Microbiota and Tryptophan Metabolites in the Remote Effect of Intestinal Inflammation on Brain and Depression
by Barbora Waclawiková and Sahar El Aidy
Pharmaceuticals 2018, 11(3), 63; https://doi.org/10.3390/ph11030063 - 25 Jun 2018
Cited by 129 | Viewed by 16775
Abstract
The human gastrointestinal tract is inhabited by trillions of commensal bacteria collectively known as the gut microbiota. Our recognition of the significance of the complex interaction between the microbiota, and its host has grown dramatically over the past years. A balanced microbial community [...] Read more.
The human gastrointestinal tract is inhabited by trillions of commensal bacteria collectively known as the gut microbiota. Our recognition of the significance of the complex interaction between the microbiota, and its host has grown dramatically over the past years. A balanced microbial community is a key regulator of the immune response, and metabolism of dietary components, which in turn, modulates several brain processes impacting mood and behavior. Consequently, it is likely that disruptions within the composition of the microbiota would remotely affect the mental state of the host. Here, we discuss how intestinal bacteria and their metabolites can orchestrate gut-associated neuroimmune mechanisms that influence mood and behavior leading to depression. In particular, we focus on microbiota-triggered gut inflammation and its implications in shifting the tryptophan metabolism towards kynurenine biosynthesis while disrupting the serotonergic signaling. We further investigate the gaps to be bridged in this exciting field of research in order to clarify our understanding of the multifaceted crosstalk in the microbiota–gut–brain interphase, bringing about novel, microbiota-targeted therapeutics for mental illnesses. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
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14 pages, 261 KiB  
Review
Inflammation and Neuro-Immune Dysregulations in Autism Spectrum Disorders
by Dario Siniscalco, Stephen Schultz, Anna Lisa Brigida and Nicola Antonucci
Pharmaceuticals 2018, 11(2), 56; https://doi.org/10.3390/ph11020056 - 4 Jun 2018
Cited by 198 | Viewed by 22595
Abstract
Autism Spectrum Disorder (ASD) is characterized by persistent deficits in social communication and interaction and restricted-repetitive patterns of behavior, interests, or activities. Strong inflammation states are associated with ASD. This inflammatory condition is often linked to immune system dysfunction. Several cell types are [...] Read more.
Autism Spectrum Disorder (ASD) is characterized by persistent deficits in social communication and interaction and restricted-repetitive patterns of behavior, interests, or activities. Strong inflammation states are associated with ASD. This inflammatory condition is often linked to immune system dysfunction. Several cell types are enrolled to trigger and sustain these processes. Neuro-inflammation and neuro-immune abnormalities have now been established in ASD as key factors in its development and maintenance. In this review, we will explore inflammatory conditions, dysfunctions in neuro-immune cross-talk, and immune system treatments in ASD management. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
399 KiB  
Review
Microglia M2A Polarization as Potential Link between Food Allergy and Autism Spectrum Disorders
by Hans O. Kalkman and Dominik Feuerbach
Pharmaceuticals 2017, 10(4), 95; https://doi.org/10.3390/ph10040095 - 9 Dec 2017
Cited by 28 | Viewed by 7719
Abstract
Atopic diseases are frequently co-morbid with autism spectrum disorders (ASD). Allergic responses are associated with an activation of mast cells, innate lymphoid cells, and Th2 cells. These cells produce type-2 cytokines (IL4 and IL13), which stimulate microglia and macrophages to adopt a phenotype [...] Read more.
Atopic diseases are frequently co-morbid with autism spectrum disorders (ASD). Allergic responses are associated with an activation of mast cells, innate lymphoid cells, and Th2 cells. These cells produce type-2 cytokines (IL4 and IL13), which stimulate microglia and macrophages to adopt a phenotype referred to as ‘alternative activation’ or ‘M2A’. M2A-polarized macrophages and microglia play a physiological role in tissue repair by secreting growth factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1. In ASD there is evidence for increased type-2 cytokines, microglia activation, M2A polarization, and increased levels of growth factors. In neurons, these growth factors drive a signal transduction pathway that leads to activation of the enzyme mammalian Target of Rapamycin (mTOR), and thereby to the inhibition of autophagy. Activation of mTOR is an effect that is also common to several of the genetic forms of autism. In the central nervous system, redundant synapses are removed via an autophagic process. Activation of mTOR would diminish the pruning of redundant synapses, which in the context of ASD is likely to be undesired. Based on this line of reasoning, atopic diseases like food allergy, eczema or asthma would represent risk factors for autism spectrum disorders. Full article
(This article belongs to the Special Issue Understanding Inflammation-induced Mental Diseases: New Opportunities for Treatment)
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