Gene networks specific for innate immunity define post-traumatic stress disorder
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The molecular factors involved in the development of Post-Traumatic Stress Disorder (PTSD) remain poorly understood. Previous transcriptomic studies investigating the mechanisms of PTSD apply targeted approaches to identify individual genes under a cross-sectional framework lack a holistic view of the behaviours and properties of these genes at the system-level. Here we sought to apply an unsupervised gene-network based approach to a prospective experimental design using whole-transcriptome RNA-Seq gene expression from peripheral blood leukocytes of U.S. Marines (N=188), obtained both pre- and post-deployment to conflict zones. We identified discrete groups of co-regulated genes (i.e., co-expression modules) and tested them for association to PTSD. We identified one module at both pre- and post-deployment containing putative causal signatures for PTSD development displaying an over-expression of genes enriched for functions of innate-immune response and interferon signalling (Type-I and Type-II). Importantly, these results were replicated in a second non-overlapping independent dataset of U.S. Marines (N=96), further outlining the role of innate immune and interferon signalling genes within co-expression modules to explain at least part of the causal pathophysiology for PTSD development. A second module, consequential of trauma exposure, contained PTSD resiliency signatures and an over-expression of genes involved in hemostasis and wound responsiveness suggesting that chronic levels of stress impair proper wound healing during/after exposure to the battlefield while highlighting the role of the hemostatic system as a clinical indicator of chronic-based stress. These findings provide novel insights for early preventative measures and advanced PTSD detection, which may lead to interventions that delay or perhaps abrogate the development of PTSD.
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Enriched expression of genes implicated in innate immunity and INF signaling at baseline pre-deployment is associated with increased risk for PTSD development post-deployment.
“In addition, enriched expression of genes implicated in innate immunity and INF signaling at baseline (pre-deployment) is associated with increased risk for PTSD development post-deployment (Breen et al, 2015).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Breen et al, 2015
Prospective studies have begun to show that higher levels of inflammation prior to trauma exposure increase risk for subsequent development of PTSD following trauma exposure.
“Although no data as yet prospectively demonstrate that chronic PTSD results in augmented inflammation, prospective studies have begun to show that higher levels of inflammation prior to trauma exposure increases risk for subsequent development of PTSD following trauma exposure (Breen et al, 2015;Eraly et al, 2014;Glatt et al, 2013;Tylee et al, 2015).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Breen et al, 2015
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Transcriptome Alterations in Posttraumatic Stress Disorder
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- Authors
- Breen, M. S., Maihofer, A. X., Glatt, S. J., Tylee, D. S., Chandler, S. D., Tsuang, M. T., Risbrough, V. B., Baker, D. G., O'Connor, D. T., Nievergelt, C. M., & Woelk, C. H.
- Affiliations
- University of Southampton (GB)
- University of California San Diego (US)
- SUNY Upstate Medical University (US)
- Corresponding author
- Breen, M S
- Nievergelt, C M
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2015-03-10
- Volume
- 20
- Issue
- 12
- Pages
- 1538-1545
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC4565790
- OpenAlex
- W2064503573
- Cited by
- 180
- References
- 57
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 8 · 2023: 10 · 2022: 20 · 2021: 16 · 2020: 15 · 2019: 19 · 2018: 19 · 2017: 29 · 2016: 24 · 2015: 5
- FWCI
- 31.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX002558)
- Brain and Behavior Research Foundation
- National Alliance for Research on Schizophrenia and Depression
- Veterans Medical Research Foundation
- Department of Science and Technology, Ministry of Science and Technology, India
- U.S. Public Health Service (R01 MHO85560)
- Office of Naval Research
- National Institute of Mental Health (R01MH085521, R01MH085560, R21MH085240, R01MH093500)
- Naval Medical Research Center (N62645)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Keywords
- post-traumatic stress disorder, gene co-expression modules, innate immunity, interferon signaling, type I interferon, interferon-gamma, peripheral blood leukocytes, Marines, hemostasis, wound healing, chronic stress, PTSD prevention
- MeSH terms
- Humans, Immunity, Innate, Male, Military Personnel, Stress Disorders, Post-Traumatic, Gene Expression, Gene Regulatory Networks, Young Adult
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