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      Protective Effect of the MCP-1 Gene Haplotype against Schizophrenia

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          Abstract

          While cytokines and their genetic variants have been intensively studied in schizophrenia, little attention has been focused on chemokines in the last years. The monocyte chemoattractant protein 1 (MCP-1) is known to attract peripheral monocytes to the brain during an inflammatory reaction and to affect the T helper (Th) cell development by stimulating Th2 polarization. Owing to the neuroinflammation in schizophrenia and the variable level of MCP-1 in these patients' sera, we proposed to analyze the impact of functional genetic variants of the MCP-1 gene (MCP-1-2518A/G (rs1024611), MCP-1-362G/C (rs2857656), and MCP-1 int1del554-567 (rs3917887)) in schizophrenic patients. We conducted a case-control study on a Tunisian population composed of 200 patients and 200 controls using RFLP-PCR. Our results indicated that the minor alleles (-2518G and Del554-567) were significantly more prevalent in controls than in patients ( P=0.001/adjusted OR = 0.42, P=0.04/adjusted OR = 0.64), whereas, for -362C minor allele, increased risk of schizophrenia was revealed ( P=0.001, adjusted OR = 2.38). In conclusion, we have identified the haplotype combination -2581G/-362G/int1del554-567 that could mediate protection against schizophrenia ( P=0.0038, OR = 0.19) and the effect could result more strongly from the MCP-1 -2582G with -362G variants, whereas the effect of int1del554-567 may in part be explained by its LD with -362.

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          Meta-analysis of cytokine alterations in schizophrenia: clinical status and antipsychotic effects.

          Brian Miller, Peter Buckley, Wesley Seabolt … (2011)
          Schizophrenia is associated with immune system dysfunction, including aberrant cytokine levels. We performed a meta-analysis of these associations, considering effects of clinical status and antipsychotic treatment following an acute illness exacerbation. We identified articles by searching PubMed, PsychInfo, and Institute for Scientific Information and the reference lists of identified studies. Forty studies met the inclusion criteria. Effect sizes were similar for studies of acutely relapsed inpatients (AR) and first-episode psychosis (FEP). Interleukin (IL)-1β, IL-6, and transforming growth factor-β (TGF-β) appeared to be state markers, as they were increased in AR and FEP (p < .001 for each) and normalized with antipsychotic treatment (p < .001, p = .008, and p = .005, respectively). In contrast, IL-12, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and soluble IL-2 receptor (sIL-2R) appeared to be trait markers, as levels remained elevated in acute exacerbations and following antipsychotic treatment. There was no difference in IL-6 levels between stable medicated outpatients and control subjects (p = .69). In the cerebrospinal fluid, IL-1β was significantly decreased in schizophrenia versus controls (p = .01). Similar effect sizes in AR and FEP suggest that the association between cytokine abnormalities and acute exacerbations of schizophrenia is independent of antipsychotic medications. While some cytokines (IL-1β, IL-6, and TGF-β) may be state markers for acute exacerbations, others (IL-12, IFN-γ, TNF-α, and sIL-2R) may be trait markers. Although these results could provide the basis for future hypothesis testing, most studies did not control for potential confounding factors such as body mass index and smoking. Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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            Neuroinflammation and psychiatric illness

            Souhel Najjar, Daniel M. Pearlman, Kenneth Alper … (2013)
            Multiple lines of evidence support the pathogenic role of neuroinflammation in psychiatric illness. While systemic autoimmune diseases are well-documented causes of neuropsychiatric disorders, synaptic autoimmune encephalitides with psychotic symptoms often go under-recognized. Parallel to the link between psychiatric symptoms and autoimmunity in autoimmune diseases, neuroimmunological abnormalities occur in classical psychiatric disorders (for example, major depressive, bipolar, schizophrenia, and obsessive-compulsive disorders). Investigations into the pathophysiology of these conditions traditionally stressed dysregulation of the glutamatergic and monoaminergic systems, but the mechanisms causing these neurotransmitter abnormalities remained elusive. We review the link between autoimmunity and neuropsychiatric disorders, and the human and experimental evidence supporting the pathogenic role of neuroinflammation in selected classical psychiatric disorders. Understanding how psychosocial, genetic, immunological and neurotransmitter systems interact can reveal pathogenic clues and help target new preventive and symptomatic therapies.
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              A novel polymorphism in the MCP-1 gene regulatory region that influences MCP-1 expression.

              Lingeng Lu, Brad H Rovin, Richa Saxena (1999)
              Two novel polymorphisms in the distal regulatory region of the MCP-1 gene were identified by directly sequencing PCR amplified genomic DNA. These polymorphisms are located at positions -2518 (G or A) and -2076 (A or T) relative to the major transcriptional start site of the gene. To examine the effect of these polymorphisms on MCP-1 transcription, polymorphic variants of the MCP-1 distal regulatory region were placed upstream of a luciferase reporter gene and transfected into A172 cells. IL-1beta-induced luciferase activity was significantly greater from cells transfected with constructs containing G at position -2518. The polymorphism at -2076 did not affect MCP-1 transcription. IL-1beta-treated peripheral blood mononuclear cells from individuals heterozygous or homozygous for G at -2518 produced more MCP-1 than cells from individuals homozygous for A at -2518. These data identify a polymorphism in the MCP-1 distal regulatory region that affects the level of MCP-1 expression in response to an inflammatory stimulus. Copyright 1999 Academic Press.
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                Author and article information

                Contributors
                Hana Saoud:
                ORCID: https://orcid.org/0000-0003-1080-4064
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2019
                Publication date (Electronic): 2 December 2019
                Volume: 2019
                Electronic Location Identifier: 4042615
                Affiliations
                1Laboratory of Genetics, Biodiversity and Bioresource Valorization, Higher Institute of Biotechnology of Monastir, University of Monastir, Monastir, Tunisia
                2Department of Epidemiology, Farhat Hached University Hospital, Sousse, Tunisia
                3Hematology Department, Fattouma Bourguiba University Hospital, TN 5000, Monastir, Tunisia
                4Department of Psychiatry and Vulnerability to Psychoses Laboratory-CHU Monastir, University of Monastir, Monastir, Tunisia
                Author notes

                Academic Editor: Milton O. Moraes

                Author information
                https://orcid.org/0000-0003-1080-4064
                https://orcid.org/0000-0002-4661-3158
                https://orcid.org/0000-0003-2316-0667
                Article
                DOI: 10.1155/2019/4042615
                PMC ID: 6925699
                PubMed ID: 31886209
                SO-VID: 0003fe6c-3903-45ce-89d3-fc8d46f3fd68
                Copyright © Copyright © 2019 Hana Saoud et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 13 August 2019
                Date revision received : 28 October 2019
                Date accepted : 15 November 2019
                Funding
                Funded by: Ministry of Higher Education, Scientific Research and Technology of Tunisia
                Categories
                Subject: Research Article

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