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      Neuropsychiatric Disease and Treatment (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on all aspects of neuropsychiatric and neurological disorders. Sign up for email alerts here.

      63,741 Monthly downloads/views I 2.989 Impact Factor I 4.5 CiteScore I 1.09 Source Normalized Impact per Paper (SNIP) I 0.744 Scimago Journal & Country Rank (SJR)

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      Plasma levels of IL-6 in patients with untreated major depressive disorder: comparison with catecholamine metabolites

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          IL-6 and catecholamines play roles in the pathophysiology of major depressive disorder (MDD).

          Aim

          The present study investigated associations between plasma IL-6 and plasma catecholamine metabolites in patients with MDD.

          Participants and methods

          A total of 148 patients (male/female 65/83, age 49.5±12.1 years) who met the criteria for MDD based on the Diagnostic and Statistical Manual of Mental Disorders IV and 40 participants as healthy controls (HC; male/female 23/17, age 44.0±10.5 years) were enrolled in the present study. Plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) were analyzed using high-performance liquid chromatography, and plasma IL-6 levels were measured using ELISA.

          Results

          No correlations were observed among plasma IL-6 levels, MHPG levels, and HVA levels in patients with MDD. Plasma IL-6 levels in patients with MDD were significantly higher than in the HC. A positive correlation was found between plasma IL-6 levels and Hamilton Rating Scale for Depression-17 scores.

          Conclusion

          No correlations existed between plasma IL-6 levels and plasma catecholamine metabolite levels in patients with MDD, and the severity of depressive state was related to plasma IL-6 levels in MDD.

          Most cited references39

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          Inflammation is associated with decreased functional connectivity within corticostriatal reward circuitry in depression

          Jennifer C. Felger, Zhihao Li, A. Haroon … (2015)
          Depression is associated with alterations in corticostriatal reward circuitry. One pathophysiologic pathway that may drive these changes is inflammation. Biomarkers of inflammation (e.g. cytokines and C-reactive protein [CRP]) are reliably elevated in depressed patients. Moreover, administration of inflammatory stimuli reduces neural activity and dopamine release in reward-related brain regions in association with reduced motivation and anhedonia. Accordingly, we examined whether increased inflammation in depression affects corticostriatal reward circuitry to lead to deficits in motivation and goal-directed motor behavior. Resting-state functional magnetic resonance imaging was conducted on 48 medically-stable, unmedicated outpatients with major depression. Whole-brain, voxel-wise functional connectivity was examined as a function of CRP using seeds for subdivisions of the ventral and dorsal striatum associated with motivation and motor control. Increased CRP was associated with decreased connectivity between ventral striatum and ventromedial prefrontal cortex (vmPFC)(corrected P<0.05), which in turn correlated with increased anhedonia (R=−0.47, P=0.001). Increased CRP similarly predicted decreased dorsal striatal to vmPFC and pre-supplementary motor area connectivity, which correlated with decreased motor speed (R=0.31 to 0.45, P<0.05) and increased psychomotor slowing (R=−0.35, P=0.015). Of note, mediation analyses revealed that these effects of CRP on connectivity mediated significant relationships between CRP and anhedonia and motor slowing. Finally, connectivity between striatum and vmPFC was associated with increased plasma interleukin (IL)-6, IL-1beta and IL-1 receptor antagonist (R=−0.33 to −0.36, P<0.05). These findings suggest that decreased corticostriatal connectivity may serve as a target for anti-inflammatory or pro-dopaminergic treatment strategies to improve motivational and motor deficits in patients with increased inflammation including depression.
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            Monoamine neurocircuitry in depression and strategies for new treatments.

            Michel Hamon, Pierre Blier (2013)
            Extensive studies showed that monoaminergic neurotransmission that involves serotonin (5-HT), norepinephrine (NE) and dopamine (DA) exerts major influence on brain circuits concerned by the regulation of mood, reactivity to psychological stress, self-control, motivation, drive, and cognitive performance. Antidepressants targeting monoamines directly affect the functional tone of these circuits, notably in limbic and frontocortical areas, and evidence has been provided that this action plays a key role in their therapeutic efficacy. Indeed, at least some of functional changes detected by functional magnetic resonance imaging in emotion- and cognitive-related circuits such as the one involving limbic-cortical-striatal-pallidal-thalamic connections in depressed patients can be reversed by monoamine-targeted antidepressants. However, antidepressants acting selectively on only one monoamine, such as selective inhibitors of 5-HT or NE reuptake, alleviate depression symptoms in a limited percentage of patients, and are poorly effective to prevent recurrence. Thorough investigations for the last 30 years allowed the demonstration of the existence of functional interactions between 5-HT, NE and DA systems, and the identification of the specific receptors involved. In particular, 5-HT systems were shown to exert negative influence on NE and DA systems through 5-HT2A and 5-HT2C receptor- mediated mechanisms, respectively. On the other hand, complex positive and negative influences of NE system on 5-HT neurotransmission are mediated through α1- and α2-adrenergic receptors, respectively. These data provided a rationale for the design of new, multimodal, therapeutic strategies involving drugs acting not only at the "historical" targets such as the 5-HT and/or the NE transporter, but also at other molecular targets to improve their efficacy and their tolerability. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Activation of central nervous system inflammatory pathways by interferon-alpha: relationship to monoamines and depression.

              J Vogt, Bettina Drake, Matthias Majer … (2009)
              Interferon (IFN)-alpha has been used to study the effects of innate immune cytokines on the brain and behavior in humans. The degree to which peripheral administration of IFN-alpha accesses the brain and is associated with a central nervous system (CNS) inflammatory response is unknown. Moreover, the relationship among IFN-alpha-associated CNS inflammatory responses, neurotransmitter metabolism, and behavior has yet to be established. Twenty-four patients with hepatitis C underwent lumbar puncture and blood sampling after approximately 12 weeks of either no treatment (n = 12) or treatment with pegylated IFN-alpha 2b (n = 12). Cerebrospinal fluid (CSF) and blood samples were analyzed for proinflammatory cytokines and their receptors as well as the chemokine, monocyte chemoattractant protein-1 (MCP-1), and IFN-alpha. Cerebrospinal fluid samples were additionally analyzed for monoamine metabolites and corticotropin releasing hormone. Depressive symptoms were assessed using the Montgomery Asberg Depression Rating Scale. Interferon-alpha was detected in the CSF of all IFN-alpha-treated patients and only one control subject. Despite no increases in plasma IL-6, IFN-alpha-treated patients exhibited significant elevations in CSF IL-6 and MCP-1, both of which were highly correlated with CSF IFN-alpha concentrations. Of the immunologic and neurotransmitter variables, log-transformed CSF concentrations of the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were the strongest predictor of depressive symptoms. Log-transformed CSF concentrations of IL-6, but not IFN-alpha or MCP-1, were negatively correlated with log-transformed CSF 5-HIAA (r(2) = -.25, p < .05). These data indicate that a peripherally administered cytokine can activate a CNS inflammatory response in humans that interacts with monoamine (serotonin) metabolism, which is associated with depression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neuropsychiatr Dis Treat
                Journal ID (iso-abbrev): Neuropsychiatr Dis Treat
                Journal ID (publisher-id): NDT
                Journal ID (pmc): neurodist
                Title: Neuropsychiatric Disease and Treatment
                Publisher: Dove
                ISSN (Print): 1176-6328
                ISSN (Electronic): 1178-2021
                Publication date (Electronic): 13 September 2019
                Publication date Collection: 2019
                Volume: 15
                Pages: 2655-2661
                Affiliations
                [1 ] Department of Psychiatry, University of Occupational and Environmental Health , Kitakyushu, Fukuoka 8078555, Japan
                [2 ] Department of Psychiatry, Fujita Medical University , Toyoake Aichi 4701192, Japan
                Author notes
                Correspondence: Reiji YoshimuraDepartment of Psychiatry, University of Occupational and Environmental Health , KitakyushuFukuoka8078555, JapanTell +81936917253Email yoshi621@med.uoeh-u.ac.jp
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 195379
                DOI: 10.2147/NDT.S195379
                PMC ID: 6752655
                SO-VID: b0cba3da-3867-46f6-9448-36566162bf89
                Copyright © © 2019 Yoshimura et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 20 November 2018
                Date accepted : 29 January 2019
                Page count
                Figures: 4, Tables: 6, References: 47, Pages: 7
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Neurology
                Keywords: il-6,3-methoxy-4-hydroxyphenylglycol,homovanillic acid,major depressive disorder,hamilton rating scale for depression
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: il-6, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, major depressive disorder, hamilton rating scale for depression

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