| Autor: |
Núñez-Rios DL; Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA.; VA CT Healthcare Center, West Haven, CT 06516, USA., Martínez-Magaña JJ; Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA.; VA CT Healthcare Center, West Haven, CT 06516, USA., Nagamatsu ST; Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA.; VA CT Healthcare Center, West Haven, CT 06516, USA., Andrade-Brito DE; Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA.; VA CT Healthcare Center, West Haven, CT 06516, USA., Forero DA; Health and Sport Sciences Research Group, School of Health and Sport Sciences, Fundación Universitaria del Área Andina, Bogotá 110231, Colombia., Orozco-Castaño CA; Health and Sport Sciences Research Group, School of Health and Sport Sciences, Fundación Universitaria del Área Andina, Bogotá 110231, Colombia., Montalvo-Ortiz JL; Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA.; VA CT Healthcare Center, West Haven, CT 06516, USA. |
| Abstrakt: |
Posttraumatic stress disorder (PTSD) is a chronic and multifactorial disorder with a prevalence ranging between 6-10% in the general population and ~35% in individuals with high lifetime trauma exposure. Growing evidence indicates that the immune system may contribute to the etiology of PTSD, suggesting the inflammatory dysregulation as a hallmark feature of PTSD. However, the potential interplay between the central and peripheral immune system, as well as the biological mechanisms underlying this dysregulation remain poorly understood. The activation of the HPA axis after trauma exposure and the subsequent activation of the inflammatory system mediated by glucocorticoids is the most common mechanism that orchestrates an exacerbated immunological response in PTSD. Recent high-throughput analyses in peripheral and brain tissue from both humans with and animal models of PTSD have found that changes in gene regulation via epigenetic alterations may participate in the impaired inflammatory signaling in PTSD. The goal of this review is to assess the role of the inflammatory system in PTSD across tissue and species, with a particular focus on the genomics, transcriptomics, epigenomics, and proteomics domains. We conducted an integrative multi-omics approach identifying TNF (Tumor Necrosis Factor) signaling, interleukins, chemokines, Toll-like receptors and glucocorticoids among the common dysregulated pathways in both central and peripheral immune systems in PTSD and propose potential novel drug targets for PTSD treatment. |
