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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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      Association between toll-like receptor 4 expression and symptoms of major depressive disorder

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          Abstract

          Background

          In our previous study, toll-like receptor 4 (TLR4) mRNA expression level was associated with severity of major depressive disorder (MDD) evaluated with the 17-item Hamilton Depression Rating Scale (HAMD-17). However, there are few studies that have investigated the relationship between symptoms of MDD and changes in TLR4 expression. Therefore, the aim of the present study was to further analyze the association between subscales of HAMD-17 and TLR4.

          Methods

          Fifty-one patients with MDD (15 male and 36 female) participated in this study. HAMD-17 was used to assess the symptoms of major depression. The mRNA expression levels of TLR4 were examined in parallel with a housekeeping gene, using real-time polymerase chain reaction. A stepwise linear regression forward model was used to evaluate the relationships between items of HAMD-17 and TLR4 expression.

          Results

          Some sickness behavior-associated symptoms, including suicide, somatic symptoms of anxiety, or performance of work and activities, were not associated with TLR4 expression. However, psychological signs of anxiety and loss of weight in HAMD-17 can predict the expression level of TLR4.

          Conclusion

          Our results suggest a significant association between anxiety, body weight loss, and TLR4 mRNA levels in patients with MDD. Larger longitudinal studies combining both subjective and objective measures of depression are needed to clarify the link between TLR4 and symptoms of depression.

          Most cited references25

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          TLR signaling.

          Taro Kawai, Shizuo Akira (2007)
          The TLR family senses the molecular signatures of microbial pathogens, and plays a fundamental role in innate immune responses. TLRs signal via a common pathway that leads to the expression of diverse inflammatory genes. In addition, each TLR elicits specific cellular responses to pathogens owing to differential usage of intracellular adapter proteins. Recent studies have revealed the importance of the subcellular localization of TLRs in pathogen recognition and signaling. TLR signaling pathways is negatively regulated by a number of cellular proteins to attenuate inflammation. Here, we describe recent advances in our understanding of the regulation of TLR-mediated signaling.
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            Immunological aspects in the neurobiology of suicide: elevated microglial density in schizophrenia and depression is associated with suicide.

            Johann Steiner, Hendrik Bielau, Ralf Brisch … (2008)
            Suicide has a high prevalence in patients with schizophrenia and affective disorder. Our recent postmortem study [Steiner J, Mawrin C, Ziegeler A, Bielau H, Ullrich O, Bernstein HG, Bogerts B. Distribution of HLA-DR-positive microglia in schizophrenia reflects impaired cerebral lateralization. Acta Neuropathologica (Berl) 2006;112:305-16.] revealed increased microglial densities in two schizophrenic patients who had committed suicide. Therefore, the hypothesis of microglial activation during acute psychosis was proposed. Alternatively, "suicide" could be a diagnosis-independent factor leading to microgliosis. To clarify this question, microglial HLA-DR expression was analyzed by immunohistochemistry in the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), mediodorsal thalamus (MD) and hippocampus of 16 schizophrenics, 14 depressed patients with affective disorder and 10 matched controls. A subgroup of six schizophrenics and seven patients with affective disorder who committed suicide was included. ANOVA revealed no effect of diagnosis on microglial density (DLPFC: P=0.469; ACC: P=0.349; MD: P=0.569; hippocampus: P=0.497). However, significant microgliosis was observed in the DLPFC (P=0.004), ACC (P=0.012) and MD (P=0.004) of suicide patients. A similar trend was seen in the hippocampus (P=0.057). In conclusion, immunological factors may play a hitherto underestimated role in suicide. First, microglial activation might be interpreted as a consequence of presuicidal stress. Second, one might speculate a causal link between microglial activation and suicidal behaviour, such as neuroendocrine factors, cytokines, and nitric oxide, which are released from microglial cells and are known to modulate noradrenergic or serotonergic neurotransmission and thus may trigger suicidality.
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              The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression.

              Michael Maes, Marta Kubera, Jean-Claude Leunis (2008)
              There is now evidence that major depression (MDD) is accompanied by an activation of the inflammatory response system (IRS) and that pro-inflammatory cytokines and lipopolysacharide (LPS) may induce depressive symptoms. The aim of the present study was to examine whether an increased gastrointestinal permeability with an increased translocation of LPS from gram negative bacteria may play a role in the pathophysiology of MDD. Toward this end, the present study examines the serum concentrations of IgM and IgA against LPS of the gram-negative enterobacteria, Hafnia Alvei, Pseudomonas Aeruginosa, Morganella Morganii, Pseudomonas Putida, Citrobacter Koseri, and Klebsielle Pneumoniae in MDD patients and normal controls. We found that the prevalences and median values for serum IgM and IgA against LPS of enterobacteria are significantly greater in patients with MDD than in normal volunteers. These differences are significant to the extent that a significant diagnostic performance is obtained, i.e. the area under the ROC curve is 90.1%. The symptom profiles of increased IgM and IgA levels are fatigue, autonomic and gastro-intestinal symptoms and a subjective feeling of infection. The results show that intestinal mucosal dysfunction characterized by an increased translocation of gram-negative bacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. It is suggested that the increased LPS translocation may mount an immune response and thus IRS activation in some patients with MDD and may induce specific "sickness behaviour" symptoms. It is suggested that patients with MDD should be checked for leaky gut by means of the IgM and IgA panel used in the present study and accordingly should be treated for leaky gut.
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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): Neuropsychiatric Disease and Treatment
                Title: Neuropsychiatric Disease and Treatment
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6328
                ISSN (Electronic): 1178-2021
                Publication date Collection: 2015
                Publication date (Electronic): 30 July 2015
                Volume: 11
                Pages: 1853-1857
                Affiliations
                [1 ]Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
                [2 ]Genomic and Proteomic Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
                [3 ]Department of Nursing, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
                [4 ]Graduate Institute of Clinical Medical Sciences, Chang Gung University, College of Medicine, Kaohsiung, Taiwan
                Author notes
                Correspondence: Yi-Yung Hung, Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan, Tel +886 7 731 7123 Extn 6317, Fax +886 7 732 6817, Email ian670523@ 123456cgmh.org.tw
                Article
                Publisher ID: ndt-11-1853
                DOI: 10.2147/NDT.S88430
                PMC ID: 4525784
                PubMed ID: 26257523
                SO-VID: 0ea29109-51a7-443c-8146-7c95084ba10b
                Copyright © © 2015 Wu et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License
                License:

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Neurology
                Keywords: major depressive disorder,innate immune,toll-like receptor,anxiety
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: major depressive disorder, innate immune, toll-like receptor, anxiety

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