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Full-Text Articles in Medical Physiology
T-Lymphocyte Tyrosine Hydroxylase Regulates T H 17 T-Lymphocytes During Repeated Social Defeat Stress, Safwan K. Elkhatib, Cassandra M. Moshfegh, Gabrielle F. Watson, Adam J. Case
T-Lymphocyte Tyrosine Hydroxylase Regulates T H 17 T-Lymphocytes During Repeated Social Defeat Stress, Safwan K. Elkhatib, Cassandra M. Moshfegh, Gabrielle F. Watson, Adam J. Case
Journal Articles: Cellular & Integrative Physiology
Posttraumatic stress disorder (PTSD) is a debilitating psychiatric disorder which results in deleterious changes to psychological and physical health. Patients with PTSD are especially susceptible to life-threatening co-morbid inflammation-driven pathologies, such as autoimmunity, while also demonstrating increased T-helper 17 (TH17) lymphocyte-driven inflammation. While the exact mechanism of this increased inflammation is unknown, overactivity of the sympathetic nervous system is a hallmark of PTSD. Neurotransmitters of the sympathetic nervous system (i.e., catecholamines) can alter T-lymphocyte function, which we have previously demonstrated to be partially mitochondrial redox-mediated. Furthermore, we have previously elucidated that T-lymphocytes generate their own catecholamines, and strong …
Autonomic And Redox Imbalance Correlates With T-Lymphocyte Inflammation In A Model Of Chronic Social Defeat Stress, Cassandra M. Moshfegh, Safwan K. Elkhatib, Christopher W. Collins, Allison J. Kohl, Adam J. Case
Autonomic And Redox Imbalance Correlates With T-Lymphocyte Inflammation In A Model Of Chronic Social Defeat Stress, Cassandra M. Moshfegh, Safwan K. Elkhatib, Christopher W. Collins, Allison J. Kohl, Adam J. Case
Journal Articles: Cellular & Integrative Physiology
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 …