Sympathetic Nerves Control Splenic T-Lymphocyte Inflammation and the Mitochondrial Redox Environment During Repeated Social Defeat Stress

Abstract

Post-traumatic stress disorder (PTSD) is a devastating psychological disorder that increases the risk for autoimmune disease by >3 fold, with the exact etiology still unclear. A known hallmark of PTSD is increased sympathetic tone and norepinephrine (NE) outflow. We have previously demonstrated that exogenous NE induces a pro-inflammatory T-helper 17 (TH17) phenotype in T-lymphocytes through a mitochondrial superoxide-dependent manner. Therefore, we hypothesized sympathetic-driven neuroimmune interactions could mediate psychological trauma-induced T-lymphocyte inflammation.