Chunk #75 — Comorbidity of Post-traumatic stress disorder or major depressive disorder with alcohol use disorder and immune signaling — Post-traumatic stress disorder and alcohol use disorder
cytokine expression, and the presence of psychiatric symptoms is a significant predictor of increased levels of cytokine expression (Tursich et al., 2014). Moreover, circulating levels of IL-1β and IL-6 positively correlate with PTSD duration and severity, respectively (Lohr et al., 2015). Whole-transcriptome RNA-seq analysis of blood leukocytes from military personnel indicate widespread changes in immune signaling modules (Breen et al., 2015; Guardado et al., 2016). Furthermore, an RNA-seq comparison of marines, before and after deployment, who developed PTSD indicates that dysregulation in innate immune signaling is not only a consequence of trauma exposure, but is significantly associated with the development of PTSD (Breen et al., 2015). In addition, genetic polymorphisms in immune regulators including TNF-α are associated with PTSD (Wang et al., 2017). Preclinical research suggests that stress and alcohol exposure interact to increase plasma endotoxins and enhance microglial activation (Walter et al., 2017). On a clinical level, many of the cytokines increased in PTSD patients also have altered expression in post-mortem brains of human alcoholics. These findings support a role for immune signaling in the pathophysiology of PTSD. However, more studies are required to determine the mechanisms and extent of peripheral vs. neuroimmune dysregulation in patients with PTSD (Olff
