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Depressive symptoms and immune transcriptional profiles in late adolescents
•Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes,...
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| Published in: | Brain, behavior, and immunity behavior, and immunity, 2019-08, Vol.80, p.163-169 |
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| container_title | Brain, behavior, and immunity |
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| creator | Chiang, Jessica J. Cole, Steve W. Bower, Julienne E. Irwin, Michael R. Taylor, Shelley E. Arevalo, Jesusa Fuligni, Andrew J. |
| description | •Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes, B cells, and dendritic cells.
Rates of depression increase and peak during late adolescence and alterations in immune processes are thought to be both a risk factor and outcome of depression. However, few studies have examined depression-immune dynamics among adolescents. Using a functional genomics approach, the current study examined whether depressive symptoms were associated with activation of a gene expression profile, characterized by upregulated expression of pro-inflammatory-related genes and downregulated expression of antiviral-related genes in a sample of older adolescents (Mage = 18.37, SD = 0.51).
Participants (n = 87) reported on their depressive symptoms during the past week using the CES-D, and provided blood samples for genome-wide transcriptional profiling of mRNA.
Adolescents with clinically-significant levels of depressive symptoms (CES-D ≥ 16) exhibited upregulated expression of inflammation-related genes and downregulated expression of antiviral-related genes compared to their peers with lower levels of depressive symptoms (CES-D |
| doi_str_mv | 10.1016/j.bbi.2019.03.004 |
| format | article |
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Rates of depression increase and peak during late adolescence and alterations in immune processes are thought to be both a risk factor and outcome of depression. However, few studies have examined depression-immune dynamics among adolescents. Using a functional genomics approach, the current study examined whether depressive symptoms were associated with activation of a gene expression profile, characterized by upregulated expression of pro-inflammatory-related genes and downregulated expression of antiviral-related genes in a sample of older adolescents (Mage = 18.37, SD = 0.51).
Participants (n = 87) reported on their depressive symptoms during the past week using the CES-D, and provided blood samples for genome-wide transcriptional profiling of mRNA.
Adolescents with clinically-significant levels of depressive symptoms (CES-D ≥ 16) exhibited upregulated expression of inflammation-related genes and downregulated expression of antiviral-related genes compared to their peers with lower levels of depressive symptoms (CES-D < 16). Bioinformatics analyses suggested that this pattern of differential gene expression was mediated by greater activity of the pro-inflammatory transcription factor, nuclear factor-kappa B (NF-κB), and reduced activity of glucocorticoid receptors (GRs) and interferon response factors (IRFs). Additional analyses implicated monocytes, B cells, and dendritic cells as primary cellular sources of the observed gene expression patterns associated with depressive symptoms.
Results are consistent with past work demonstrating links between depression and altered immunity. They provide a molecular basis for these associations and suggest that the underlying molecular signature may emerge as early as late adolescence when rates of depression tend to increase.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2019.03.004</identifier><identifier>PMID: 30851376</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adolescent ; Depression - genetics ; Depression - immunology ; Depression - metabolism ; Depressive Disorder - immunology ; Depressive Disorder - metabolism ; Female ; Gene Expression Profiling - methods ; Gene Expression Regulation - genetics ; Genomics - methods ; Humans ; Inflammation - blood ; Male ; NF-kappa B - genetics ; Receptors, Glucocorticoid - genetics ; Transcriptome - genetics ; Young Adult</subject><ispartof>Brain, behavior, and immunity, 2019-08, Vol.80, p.163-169</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-7501e5fa5b2a84a7eb5e7ad31350851b6e1f408164a0d526b066f7abf5fab6903</citedby><cites>FETCH-LOGICAL-c451t-7501e5fa5b2a84a7eb5e7ad31350851b6e1f408164a0d526b066f7abf5fab6903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,783,787,888,27936,27937</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30851376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chiang, Jessica J.</creatorcontrib><creatorcontrib>Cole, Steve W.</creatorcontrib><creatorcontrib>Bower, Julienne E.</creatorcontrib><creatorcontrib>Irwin, Michael R.</creatorcontrib><creatorcontrib>Taylor, Shelley E.</creatorcontrib><creatorcontrib>Arevalo, Jesusa</creatorcontrib><creatorcontrib>Fuligni, Andrew J.</creatorcontrib><title>Depressive symptoms and immune transcriptional profiles in late adolescents</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>•Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes, B cells, and dendritic cells.
Rates of depression increase and peak during late adolescence and alterations in immune processes are thought to be both a risk factor and outcome of depression. However, few studies have examined depression-immune dynamics among adolescents. Using a functional genomics approach, the current study examined whether depressive symptoms were associated with activation of a gene expression profile, characterized by upregulated expression of pro-inflammatory-related genes and downregulated expression of antiviral-related genes in a sample of older adolescents (Mage = 18.37, SD = 0.51).
Participants (n = 87) reported on their depressive symptoms during the past week using the CES-D, and provided blood samples for genome-wide transcriptional profiling of mRNA.
Adolescents with clinically-significant levels of depressive symptoms (CES-D ≥ 16) exhibited upregulated expression of inflammation-related genes and downregulated expression of antiviral-related genes compared to their peers with lower levels of depressive symptoms (CES-D < 16). Bioinformatics analyses suggested that this pattern of differential gene expression was mediated by greater activity of the pro-inflammatory transcription factor, nuclear factor-kappa B (NF-κB), and reduced activity of glucocorticoid receptors (GRs) and interferon response factors (IRFs). Additional analyses implicated monocytes, B cells, and dendritic cells as primary cellular sources of the observed gene expression patterns associated with depressive symptoms.
Results are consistent with past work demonstrating links between depression and altered immunity. They provide a molecular basis for these associations and suggest that the underlying molecular signature may emerge as early as late adolescence when rates of depression tend to increase.</description><subject>Adolescent</subject><subject>Depression - genetics</subject><subject>Depression - immunology</subject><subject>Depression - metabolism</subject><subject>Depressive Disorder - immunology</subject><subject>Depressive Disorder - metabolism</subject><subject>Female</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation - genetics</subject><subject>Genomics - methods</subject><subject>Humans</subject><subject>Inflammation - blood</subject><subject>Male</subject><subject>NF-kappa B - genetics</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Transcriptome - genetics</subject><subject>Young Adult</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9UcFO3DAQtVCrskA_gEuVYy9JZ-LYSVSpElpaiorEBc6WnUzAq8RO7exK_D1eLUXlwmk0mvfevJnH2DlCgYDy26YwxhYlYFsALwCqI7ZCaCEvkbcf2Aqaps1RtHjMTmLcAIDg2HxixxwagbyWK_bnkuZAMdodZfFpmhc_xUy7PrPTtHWULUG72AU7L9Y7PWZz8IMdKWbWZaNeKNO9T21Hboln7OOgx0ifX-opu__18279O7-5vbpeX9zkXSVwyWsBSGLQwpS6qXRNRlCte45c7G0ZSThU0KCsNPSilAakHGpthsQxsgV-yn4cdOetmajf7w56VHOwkw5Pymur3k6cfVQPfqdkjQBYJoGvLwLB_91SXNRk0wnjqB35bVQlNq2osJYyQfEA7YKPMdDwugZB7UNQG5VCUPsQFHCVQkicL__7e2X8-3oCfD8AKH1pZymo2FlyHfU2ULeo3tt35J8BLgSZnA</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Chiang, Jessica J.</creator><creator>Cole, Steve W.</creator><creator>Bower, Julienne E.</creator><creator>Irwin, Michael R.</creator><creator>Taylor, Shelley E.</creator><creator>Arevalo, Jesusa</creator><creator>Fuligni, Andrew J.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190801</creationdate><title>Depressive symptoms and immune transcriptional profiles in late adolescents</title><author>Chiang, Jessica J. ; Cole, Steve W. ; Bower, Julienne E. ; Irwin, Michael R. ; Taylor, Shelley E. ; Arevalo, Jesusa ; Fuligni, Andrew J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-7501e5fa5b2a84a7eb5e7ad31350851b6e1f408164a0d526b066f7abf5fab6903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adolescent</topic><topic>Depression - genetics</topic><topic>Depression - immunology</topic><topic>Depression - metabolism</topic><topic>Depressive Disorder - immunology</topic><topic>Depressive Disorder - metabolism</topic><topic>Female</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation - genetics</topic><topic>Genomics - methods</topic><topic>Humans</topic><topic>Inflammation - blood</topic><topic>Male</topic><topic>NF-kappa B - genetics</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Transcriptome - genetics</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chiang, Jessica J.</creatorcontrib><creatorcontrib>Cole, Steve W.</creatorcontrib><creatorcontrib>Bower, Julienne E.</creatorcontrib><creatorcontrib>Irwin, Michael R.</creatorcontrib><creatorcontrib>Taylor, Shelley E.</creatorcontrib><creatorcontrib>Arevalo, Jesusa</creatorcontrib><creatorcontrib>Fuligni, Andrew J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain, behavior, and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chiang, Jessica J.</au><au>Cole, Steve W.</au><au>Bower, Julienne E.</au><au>Irwin, Michael R.</au><au>Taylor, Shelley E.</au><au>Arevalo, Jesusa</au><au>Fuligni, Andrew J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Depressive symptoms and immune transcriptional profiles in late adolescents</atitle><jtitle>Brain, behavior, and immunity</jtitle><addtitle>Brain Behav Immun</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>80</volume><spage>163</spage><epage>169</epage><pages>163-169</pages><issn>0889-1591</issn><eissn>1090-2139</eissn><abstract>•Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes, B cells, and dendritic cells.
Rates of depression increase and peak during late adolescence and alterations in immune processes are thought to be both a risk factor and outcome of depression. However, few studies have examined depression-immune dynamics among adolescents. Using a functional genomics approach, the current study examined whether depressive symptoms were associated with activation of a gene expression profile, characterized by upregulated expression of pro-inflammatory-related genes and downregulated expression of antiviral-related genes in a sample of older adolescents (Mage = 18.37, SD = 0.51).
Participants (n = 87) reported on their depressive symptoms during the past week using the CES-D, and provided blood samples for genome-wide transcriptional profiling of mRNA.
Adolescents with clinically-significant levels of depressive symptoms (CES-D ≥ 16) exhibited upregulated expression of inflammation-related genes and downregulated expression of antiviral-related genes compared to their peers with lower levels of depressive symptoms (CES-D < 16). Bioinformatics analyses suggested that this pattern of differential gene expression was mediated by greater activity of the pro-inflammatory transcription factor, nuclear factor-kappa B (NF-κB), and reduced activity of glucocorticoid receptors (GRs) and interferon response factors (IRFs). Additional analyses implicated monocytes, B cells, and dendritic cells as primary cellular sources of the observed gene expression patterns associated with depressive symptoms.
Results are consistent with past work demonstrating links between depression and altered immunity. They provide a molecular basis for these associations and suggest that the underlying molecular signature may emerge as early as late adolescence when rates of depression tend to increase.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30851376</pmid><doi>10.1016/j.bbi.2019.03.004</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Depression - genetics Depression - immunology Depression - metabolism Depressive Disorder - immunology Depressive Disorder - metabolism Female Gene Expression Profiling - methods Gene Expression Regulation - genetics Genomics - methods Humans Inflammation - blood Male NF-kappa B - genetics Receptors, Glucocorticoid - genetics Transcriptome - genetics Young Adult |
| title | Depressive symptoms and immune transcriptional profiles in late adolescents |
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