Symptom severity predicts degree of T cell activation in adult women following childhood maltreatment

Lemieux, Andrine; Coe, Christopher L.; Carnes, Molly

doi:10.1016/j.bbi.2008.02.005

Cited by 70 publications

(52 citation statements)

References 56 publications

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“…Individuals with PTSD also have reduced numbers of naive CD8(+) T lymphocytes and increases in the proportions of CD3(+) central and effector memory T lymphocytes compared with individuals without PTSD (Sommershof et al, 2009). Furthermore, higher levels of CD4 and CD5 expression (a marker of early immune response activation; Lemieux et al, 2008) on T cells is correlated positively with intrusive and negatively with avoidant symptoms in women with PTSD (Lemieux et al, 2008). Individuals with PTSD also exhibit increases in total PBMCs, pro-inflammatory Th1 and Th17 cells, and decreased T-regulatory (T-reg) cells that are correlated with increased peripheral concentrations of IFN-γ and IL-17 (Zhou et al, 2014).…”

Section: Ptsd and Inflammationmentioning

confidence: 99%

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

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

545

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

545

376

View full text Add to dashboard Cite

show abstract

“…Further evidence of altered immune function in PTSD has been demonstrated in studies showing that the numbers of leukocytes and lymphocytes, as well as early activation markers of T lymphocytes such as CD45RA, are elevated in PTSD (29,61,107). Moreover, numbers of T regulatory cells, which are involved in suppressing inflammatory T lymphocyte responses, are significantly reduced (99).…”

Section: Autonomic-immune Dysfunction In Ptsdmentioning

confidence: 99%

Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease

Brudey

Park

Wiaderkiewicz

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

107

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-Stressand anxiety-related disorders are on the rise in both military and general populations. Over the next decade, it is predicted that treatment of these conditions, in particular, posttraumatic stress disorder (PTSD), along with its associated longterm comorbidities, will challenge the health care system. Multiple organ systems are adversely affected by PTSD, and PTSD is linked to cancer, arthritis, digestive disease, and cardiovascular disease. Evidence for a strong link between PTSD and cardiovascular disease is compelling, and this review describes current clinical data linking PTSD to cardiovascular disease, via inflammation, autonomic dysfunction, and the renin-angiotensin system. Recent clinical and preclinical evidence regarding the role of the renin-angiotensin system in the extinction of fear memory and relevance in PTSD-related immune and autonomic dysfunction is also addressed. posttraumatic stress disorder; cardiovascular disease; renin-angiotensin system POSTTRAUMATIC STRESS DISORDER (PTSD) is a psychiatric illness characterized by persistent emotional and mental stress following a traumatic event. Symptoms of PTSD include hyperarousal, flashbacks, intrusive thoughts, or nightmares, and avoidance of activities that trigger memories of the traumatic event. The health consequences of PTSD are substantial, affecting multiple organ systems, with evidence linking PTSD to diseases such as cancer, arthritis, digestive disease, and cardiovascular disease (CVD) (13,14,112). The evidence demonstrating increased risk for CVD in PTSD (9,15,19,49,57,58) is compelling, and several excellent recent review articles have highlighted this association (20,23,52,63,112). While this association could certainly be due, in part, to related unhealthy behaviors, such as increased prevalence of smoking, poor diet, and physical inactivity (46,119). Yet even after adjustments for lifestyle, comorbid conditions, and combat engagements in multivariate models, PTSD remains a significant and independent risk factor for the development of CVD and CVD-related mortality (15).Increased CVD risk in PTSD has been demonstrated in both military (21) and civilian populations (44,82). A co-twin study design (monozygotic and dizygotic), which controlled for genetic and familial confounders, demonstrated that the incidence of coronary heart disease was more than double in Vietnam War veteran twins with PTSD (22.6%) compared with those without PTSD (8.9%) (106). Most recently, one of the largest longitudinal studies examining the association between PTSD and heart failure was completed, and veterans with PTSD were shown to be nearly 50% more likely to develop heart failure than veterans without PTSD (91). This remained significant after adjustments for age, sex, diabetes, hyperlipidemia, hypertension, body mass index, combat, and military service. Civilian PTSD populations are also at greater risk for CVD. Following life-threatening traumatic events such as earthquakes (82), the 9 -11 World Trade Center attack (45), and living in urban dis...

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“…One study indicated brain volume differences in specific regions were found for women abused at ages 3-5 years (hippocampus) versus ages 9-10 years (corpus callosum), ages 11-13 years (hippocampus), or 14-16 years (frontal cortex) (Andersen et al, 2008). Studies of CSA survivors categorized as having PTSD or not sometimes indicate biological dysregulation occurs only among CSA survivors with current PTSD (e.g., T cell activation of the immune system) (Lemieux, Coe, & Carnes, 2008). Functional brain imaging of CSA exposed adults with PTSD demonstrate changes in activation patterns (Lanius, Bluhm, Lanius, & Pain, 2006).…”

Section: Biological Functioning Among Adult Survivors Of Sexual Abusementioning

confidence: 99%