ArticleFrontiers in behavioral neuroscience2019
Autonomic and Redox Imbalance Correlates With T-Lymphocyte Inflammation in a Model of Chronic Social Defeat Stress.
Article in Frontiers in behavioral neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Behavioral and Biochemical Effects of Vitexin-Isovitexin-Loaded Microcapsule Combination on Restraint Stress Mouse Model.International journal of molecular sciences · 2026Article
- The neuroimmune axis and chronic pain disorders.iScience · 2026Review
- Psychological trauma increases blood pressure sensitivity to angiotensin II via T-lymphocytes independent of psychopathology.bioRxiv : the preprint server for biology · 2025Article
- Elevated LDL-C induces T-cell metabolic dysfunction and increases inflammation and oxidative stress in midlife adults.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Hemoglobin alpha is a redox-sensitive mitochondrial-related protein in T-lymphocytes.Free radical biology & medicine · 2025Article
- Psychological trauma increases blood pressure sensitivity to angiotensin II via T-lymphocytes independent of psychopathology.Frontiers in cellular neuroscience · 2025Article
- TBrain, behavior, and immunity · 2025Article
- Hemoglobin alpha is a redox-sensitive mitochondrial-related protein in T-lymphocytes.bioRxiv : the preprint server for biology · 2024Article
- Neurobehavioral Characterization of Perinatal Oxycodone-Exposed Offspring in Early Adolescence.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Innate and adaptive immune system consequences of post-traumatic stress disorder.Autonomic neuroscience : basic & clinical · 2024Review
- Higher arterial stiffness and blunted vagal control of the heart in young women with compared to without a clinical diagnosis of PTSD.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024Article
- Repeated social defeat stress leads to immunometabolic shifts in innate immune cells of the spleen.Brain, behavior, & immunity - health · 2023Article
- S100a9 Protects Against the Effects of Repeated Social Defeat Stress.Biological psychiatry global open science · 2023Article
- Sex-specific immune mechanisms in PTSD symptomatology and risk: A translational overview and perspectives.Brain research bulletin · 2023Review
- The associations between metabolic profiles and sexual and physical abuse in depressed adolescent psychiatric outpatients: an exploratory pilot study.European journal of psychotraumatology · 2023Article
- Defining the nuanced nature of redox biology in post-traumatic stress disorder.Frontiers in physiology · 2023Review
- The role of the immune system in posttraumatic stress disorder.Translational psychiatry · 2022Review
- T-lymphocyte tyrosine hydroxylase regulates TBrain, behavior, and immunity · 2022Article
- Augmented T-cell mitochondrial reactive oxygen species in adults with major depressive disorder.American journal of physiology. Heart and circulatory physiology · 2022Article
- Interleukine-17 Modulates Neurogenesis and Behavior Following Exposure to Trauma in Mice.Cells · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Patients diagnosed with post-traumatic stress disorder (PTSD) are at a significantly elevated risk of developing comorbid inflammatory conditions, but the mechanisms underlying this predilection remain unclear. Our previous work has shown that T-lymphocytes exposed to elevated levels of norepinephrine (NE) displayed a pro-inflammatory signature reminiscent of an autoreactive phenotype. With this, we hypothesized that the increased sympathetic tone observed during psychological trauma may be promoting pro-inflammatory T-lymphocytes, which causes a predisposition to comorbid inflammatory conditions. Here, we examined the consequences of psychological trauma on splenic T-lymphocytes using a mouse model of repeated social defeat stress. Social defeat led to anxiety-like and depression-like behavior as has been previously described. The spleens of socially-defeated mice showed significant elevations of NE, tyrosine hydroxylase (TH), and acetylcholinesterase (ACHE) levels, which appeared to be due in part to increased expression within T-lymphocytes. Additionally, T-lymphocytes from stressed animals showed higher levels of pro-inflammatory cytokines and mitochondrial superoxide. Interestingly, in this model system, close associations exist within splenic T-lymphocytes amid the autonomic, inflammatory, and redox environments, but these only weakly correlate with individual behavioral differences among animals suggesting the psychological and physiological manifestations of trauma may not be tightly coupled. Last, we describe, for the first time, elevations in calprotectin levels within T-lymphocytes and in circulation of psychologically stressed animals. Calprotectin correlated with both behavioral and physiological changes after social defeat, suggesting the potential for a new biological marker and/or therapeutic target for psychological trauma and its inflammatory comorbidities.
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