Ontology highlight
ABSTRACT: Background
Post-traumatic stress disorder (PTSD) is a devastating psychological disorder. Patients with PTSD canonically demonstrate an increased risk for inflammatory diseases, as well as increased sympathetic tone and norepinephrine (NE) outflow. Yet, the exact etiology and causal nature of these physiologic changes remain unclear. Previously, we demonstrated that exogenous NE alters mitochondrial superoxide in T-lymphocytes to produce a pro-inflammatory T-helper 17 (TH17) phenotype, and observed similar TH17 polarization in a preclinical model of PTSD. Therefore, we hypothesized sympathetic-driven neuroimmune interactions could mediate psychological trauma-induced T-lymphocyte inflammation.Methods
Repeated social defeat stress (RSDS) is a preclinica
SUBMITTER: Elkhatib SK
PROVIDER: S-EPMC8941638 | biostudies-literature | 2021 Sep
REPOSITORIES: biostudies-literature