Replicable and Coupled Changes in Innate and Adaptive Immune Gene Expression in Two Case-Control Studies of Blood Microarrays in Major Depressive Disorder
Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation. We used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline–High-Throughput Disease-specific...
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| Veröffentlicht in: | Biological psychiatry (1969) Jg. 83; H. 1; S. 70 - 80 |
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| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
Elsevier Inc
01.01.2018
Elsevier |
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| ISSN: | 0006-3223, 1873-2402, 1873-2402 |
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| Abstract | Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation.
We used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline–High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen–Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold (q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance.
A total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies).
MDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression. |
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| AbstractList | AbstractBackgroundPeripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation. MethodsWe used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline–High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen–Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold ( q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance. ResultsA total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies). ConclusionsMDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression. Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation.BACKGROUNDPeripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation.We used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline-High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen-Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold (q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance.METHODSWe used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline-High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen-Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold (q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance.A total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies).RESULTSA total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies).MDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression.CONCLUSIONSMDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression. Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation. We used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline-High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen-Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold (q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance. A total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies). MDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression. |
| Author | Greene, Jonathan R. Freeman, Tom Cardinal, Rudolf Wu, Zhaozong Henderson, Robbie Drevets, Wayne Borsini, Alessandra Chandran, David Wittenberg, Gayle M. Hume, David Wittenberg, Gayle Drevets, Wayne C. Regan, Tim Perry, V. Hugh Souza-Teodoro, Luis Bullmore, Edward T. Leday, Gwenaël G.R. Richardson, Sylvia Bullmore, Edward Leday, Gwenael Cattaneo, Annamaria Vértes, Petra E. Stewart, Robert Khan, Shahid Jones, Declan Bell, Joshua Pariante, Carmine M. Pariante, Carmine Stylianou, Annie Harrison, Neil Harrison, Neil A. Zunszain, Patricia Carvalho, Livia Perry, Hugh Freeman, Tom C. Vertes, Petra |
| AuthorAffiliation | a Medical Research Council Biostatistics Unit, Cambridge, United Kingdom e ImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom f Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom i Rancho BioSciences, San Diego, California b Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom h Centre for Biological Sciences, University of Southampton, Southampton, United Kingdom d Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom g Brighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom j Janssen Research & Development, Titusville, New Jersey c Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge, United Kingdom |
| AuthorAffiliation_xml | – name: d Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom – name: e ImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom – name: c Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge, United Kingdom – name: h Centre for Biological Sciences, University of Southampton, Southampton, United Kingdom – name: i Rancho BioSciences, San Diego, California – name: b Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom – name: g Brighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom – name: a Medical Research Council Biostatistics Unit, Cambridge, United Kingdom – name: j Janssen Research & Development, Titusville, New Jersey – name: f Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom |
| Author_xml | – sequence: 1 givenname: Gwenaël G.R. surname: Leday fullname: Leday, Gwenaël G.R. organization: Medical Research Council Biostatistics Unit, Cambridge, United Kingdom – sequence: 2 givenname: Petra E. surname: Vértes fullname: Vértes, Petra E. organization: Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom – sequence: 3 givenname: Sylvia surname: Richardson fullname: Richardson, Sylvia organization: Medical Research Council Biostatistics Unit, Cambridge, United Kingdom – sequence: 4 givenname: Jonathan R. surname: Greene fullname: Greene, Jonathan R. organization: Rancho BioSciences, San Diego, California – sequence: 5 givenname: Tim surname: Regan fullname: Regan, Tim organization: Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom – sequence: 6 givenname: Shahid surname: Khan fullname: Khan, Shahid organization: ImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom – sequence: 7 givenname: Robbie surname: Henderson fullname: Henderson, Robbie organization: ImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom – sequence: 8 givenname: Tom C. surname: Freeman fullname: Freeman, Tom C. organization: Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom – sequence: 9 givenname: Carmine M. surname: Pariante fullname: Pariante, Carmine M. organization: Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom – sequence: 10 givenname: Neil A. surname: Harrison fullname: Harrison, Neil A. organization: Brighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom – sequence: 11 givenname: Edward surname: Bullmore fullname: Bullmore, Edward – sequence: 11 givenname: Edward orcidid: 0000-0002-8955-8283 surname: Bullmore fullname: Bullmore, Edward – sequence: 12 givenname: Petra surname: Vertes fullname: Vertes, Petra – sequence: 13 givenname: Rudolf surname: Cardinal fullname: Cardinal, Rudolf – sequence: 14 givenname: Sylvia surname: Richardson fullname: Richardson, Sylvia – sequence: 15 givenname: Gwenael surname: Leday fullname: Leday, Gwenael – sequence: 16 givenname: Tom surname: Freeman fullname: Freeman, Tom – sequence: 17 givenname: Tim surname: Regan fullname: Regan, Tim – sequence: 18 givenname: David surname: Hume fullname: Hume, David – sequence: 19 givenname: Zhaozong surname: Wu fullname: Wu, Zhaozong – sequence: 20 givenname: Carmine surname: Pariante fullname: Pariante, Carmine – sequence: 21 givenname: Annamaria surname: Cattaneo fullname: Cattaneo, Annamaria – sequence: 22 givenname: Patricia surname: Zunszain fullname: Zunszain, Patricia – sequence: 23 givenname: Alessandra surname: Borsini fullname: Borsini, Alessandra – sequence: 24 givenname: Robert surname: Stewart fullname: Stewart, Robert – sequence: 25 givenname: David surname: Chandran fullname: Chandran, David – sequence: 26 givenname: Livia surname: Carvalho fullname: Carvalho, Livia – sequence: 27 givenname: Joshua surname: Bell fullname: Bell, Joshua – sequence: 28 givenname: Luis surname: Souza-Teodoro fullname: Souza-Teodoro, Luis – sequence: 29 givenname: Hugh surname: Perry fullname: Perry, Hugh – sequence: 30 givenname: Neil surname: Harrison fullname: Harrison, Neil – sequence: 31 givenname: Wayne surname: Drevets fullname: Drevets, Wayne – sequence: 32 givenname: Gayle surname: Wittenberg fullname: Wittenberg, Gayle – sequence: 33 givenname: Declan surname: Jones fullname: Jones, Declan – sequence: 35 givenname: Shahid surname: Khan fullname: Khan, Shahid – sequence: 36 givenname: Annie surname: Stylianou fullname: Stylianou, Annie – sequence: 37 givenname: Robbie surname: Henderson fullname: Henderson, Robbie – sequence: 38 givenname: V. Hugh surname: Perry fullname: Perry, V. Hugh organization: Centre for Biological Sciences, University of Southampton, Southampton, United Kingdom – sequence: 39 givenname: Wayne C. surname: Drevets fullname: Drevets, Wayne C. organization: Janssen Research & Development, Titusville, New Jersey – sequence: 40 givenname: Gayle M. surname: Wittenberg fullname: Wittenberg, Gayle M. organization: Janssen Research & Development, Titusville, New Jersey – sequence: 41 givenname: Edward T. surname: Bullmore fullname: Bullmore, Edward T. email: etb23@cam.ac.uk organization: Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28688579$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Contributor | Freeman, Tom Cardinal, Rudolf Wu, Zhaozong Drevets, Wayne Henderson, Robbie Borsini, Alessandra Chandran, David Hume, David Wittenberg, Gayle Regan, Tim Souza-Teodoro, Luis Richardson, Sylvia Bullmore, Edward Leday, Gwenael Cattaneo, Annamaria Stewart, Robert Khan, Shahid Jones, Declan Bell, Joshua Pariante, Carmine Stylianou, Annie Harrison, Neil Zunszain, Patricia Carvalho, Livia Perry, Hugh Vertes, Petra |
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| Copyright | 2017 Society of Biological Psychiatry Society of Biological Psychiatry Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved. 2017 Society of Biological Psychiatry. All rights reserved. 2017 Society of Biological Psychiatry |
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| Keywords | Biomarker Inflammation Affymetrix Systems Bayesian Transcriptome |
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| Snippet | Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation.... AbstractBackgroundPeripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus... Peripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of... |
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| SubjectTerms | Affymetrix Bayesian Biomarker Biomarkers - blood Case-Control Studies Depressive Disorder, Major - blood Depressive Disorder, Major - genetics Depressive Disorder, Major - immunology Gene Expression Gene Expression Regulation Humans Immunity, Innate - genetics Inflammation Microarray Analysis Psychiatric/Mental Health Systems Transcriptome Wernicke Encephalopathy |
| Title | Replicable and Coupled Changes in Innate and Adaptive Immune Gene Expression in Two Case-Control Studies of Blood Microarrays in Major Depressive Disorder |
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