Epigenetic and immune function profiles associated with posttraumatic stress disorder
The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights i...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 20; pp. 9470 - 9475 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
18.05.2010
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Abstract | The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (n = 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV--a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes. |
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AbstractList | The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (
n
= 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV—a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes. The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (n = 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV-a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes. The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (n = 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV - a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes. [PUBLICATION ABSTRACT] |
Author | Pawelec, Graham Wildman, Derek E Galea, Sandro Koenen, Karestan C Uddin, Monica de los Santos, Regina Aiello, Allison E Goldmann, Emily |
Author_xml | – sequence: 1 fullname: Uddin, Monica – sequence: 2 fullname: Aiello, Allison E – sequence: 3 fullname: Wildman, Derek E – sequence: 4 fullname: Koenen, Karestan C – sequence: 5 fullname: Pawelec, Graham – sequence: 6 fullname: de los Santos, Regina – sequence: 7 fullname: Goldmann, Emily – sequence: 8 fullname: Galea, Sandro |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20439746$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: M.U., A.E.A., D.E.W., K.C.K., G.P., and S.G. designed research; M.U., R.d.l.S., E.G., and S.G. performed research; D.E.W. contributed new reagents/analytic tools; M.U., A.E.A., D.E.W., K.C.K., R.d.l.S., E.G., and S.G. analyzed data; and M.U., A.E.A., D.E.W., K.C.K., G.P., R.d.l.S., and S.G. wrote the paper. Edited by Burton H. Singer, Princeton University, Princeton, NJ, and approved April 1, 2010 (received for review September 21, 2009) |
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Snippet | The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system... |
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SubjectTerms | Adult Antibodies Biological Sciences Biomarkers Blood Correlation analysis CpG Islands - genetics Cytomegalovirus Cytomegalovirus Infections - immunology Disorders DNA methylation DNA Methylation - immunology Enzyme-Linked Immunosorbent Assay Epidemiology Epigenesis, Genetic - immunology Epigenetics Female Gene Expression Profiling Genes Genetics Herpesvirus Humans Immune system Male Methylation Microarray Analysis Middle Aged Military psychiatry Post traumatic stress disorder Stress Disorders, Post-Traumatic - genetics Stress Disorders, Post-Traumatic - immunology |
Title | Epigenetic and immune function profiles associated with posttraumatic stress disorder |
URI | https://www.jstor.org/stable/25681616 http://www.pnas.org/content/107/20/9470.abstract https://www.ncbi.nlm.nih.gov/pubmed/20439746 https://www.proquest.com/docview/312301868/abstract/ https://search.proquest.com/docview/733500415 https://search.proquest.com/docview/745638888 https://pubmed.ncbi.nlm.nih.gov/PMC2889041 |
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