PTSD is associated with an increase in aged T cell phenotypes in adults living in Detroit

Aiello, Allison E.; Dowd, Jennifer Beam; Jayabalasingham, Bamini; Feinstein, Lydia; Uddin, Monica; Simanek, Amanda M.; Cheng, Caroline; Galea, Sandro; Wildman, Derek E.; Koenen, Karestan C.; Pawelec, Graham

doi:10.1016/j.psyneuen.2016.01.024

Cited by 46 publications

(40 citation statements)

References 45 publications

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“…Because T-reg cells are critical for containing pro-inflammatory responses and Th1 and Th17 cells activate inflammatory responses (Afzali et al, 2007), these alterations in the composition of T-cell subsets may act in aggregate to direct systemic inflammatory tone into an overdrive state in PTSD (Jergovic et al, 2014). Finally, immunological aging of T-cell phenotypes has also been associated with PTSD (Aiello et al, 2016).…”

Section: Ptsd and Inflammationmentioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

548

376

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The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

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Section: Ptsd and Inflammationmentioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

548

376

View full text Add to dashboard Cite

show abstract

“…Aiello et al [70•] showed that PTSD was associated with lower CD4/CD8 T-cell ratios and a greater number of late-stage (relative to naïve) T-cells. These results were obtained in a sample of 85 adults with extensive community trauma histories and analyses controlled for chronological age, suggesting that PTSD might be accelerating this age-related immune process.…”

Section: Traumatic Stress and Inflammation And Immune Responsementioning

confidence: 99%

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Wolf

Morrison

2017

Curr Psychiatry Rep

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Purpose of review The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging. Recent findings Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. Summary The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress responding. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.

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“…Notably, systemic inflammation may underlie the pathophysiology of PTSD, as well as the consistent link between PTSD and chronic medical conditions associated with aging, such as cardiovascular, metabolic, autoimmune, and neurodegenerative diseases [4][5][6][7][8], and other markers of accelerated aging [6,7,[9][10][11][12][13][14]. This dysregulated inflammatory state is itself partially coordinated by maladaptive alterations of hypothalamic-pituitary adrenal (HPA) axis activity and sympathetic nervous system (SNS) sensitivity/responsivity [15,16], which affect both peripheral immune cells in blood and neuroimmune dynamics in brain.…”

Section: Introductionmentioning

confidence: 99%

Sex-specific and shared expression profiles of vulnerability and resilience to trauma in brain and blood

Kim

Uddin

2020

Biol Sex Differ

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Background: While post-traumatic stress disorder (PTSD) is defined by behavioral/cognitive symptoms most directly relevant to brain function, it can be considered a systemic disorder characterized by a distinct inability to reinstate homeostasis after trauma. Methods: In this study, we conducted a secondary analysis of gene expression profiles in key PTSD-relevant tissues, namely blood, amygdala, and hippocampus, from a rat model of PTSD, to identify sex-specific and shared processes associated with individual differences in response to recent trauma exposure. Results: Our findings suggest both shared and sex-specific mechanisms underlying individual differences associated with vulnerability and resilience to trauma in hippocampus, amygdala, and blood. By disentangling cell composition from transcriptional changes, we found higher proportions of hippocampal oligodendrocytes in the PTSD-like, extreme behavioral response (EBR) group for both sexes and also identified modules for transcriptional activity associated with group differences (i.e., response to trauma) in the hippocampus that appeared to be sex-specific. By contrast, we found prominent sex differences, but no group differences, in amygdalar cell composition, and both shared and sex-specific modules representing PTSD-relevant transcriptional activity in the amygdala. Across amygdala and hippocampus, both sex-specific and shared processes were relevant to an overarching framework for EBR implicating disrupted TNFα/NFκΒ signaling and excitatory/inhibitory imbalance in dysregulated synaptic/structural plasticity with important implications for fear learning and memory. Our main finding in peripheral blood was consistent with the human literature and identified wound healing processes and hemostasis to be upregulated in the resilient, minimal behavioral response (MBR) group across sexes, but disrupted in a sexually dimorphic manner in the EBR group. Conclusion: In contrast to the varied characterization of the PTSD-like EBR group, characterization of MBR across blood, amygdala, and hippocampus suggests a common theme of upregulated wound healing and extracellular matrix (ECM) remodeling shared between sexes. In all, we identified differential oligodendrocyte proportions in hippocampus between PTSD-like EBR and resilient MBR, and identified processes and pathways that characterize the EBR and MBRassociated transcriptional changes across hippocampus, amygdala, and blood. The sex-specific mechanisms involved in EBR may contribute to the pronounced disparity in risk for PTSD, with women much more likely to develop PTSD.

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PTSD is associated with an increase in aged T cell phenotypes in adults living in Detroit

Cited by 46 publications

References 45 publications

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Sex-specific and shared expression profiles of vulnerability and resilience to trauma in brain and blood

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