Flow cytometric determination of glucocorticoid receptor (GCR) expression in lymphocyte subpopulations: lower quantity of GCR in patients with post-traumatic stress disorder (PTSD)

Gotovac, Katja; Sabioncello, Ante; Rabatić, Sabina; Berki, Tímea; Dekaris, Dragan

doi:10.1046/j.1365-2249.2003.02075.x

Cited by 83 publications

(50 citation statements)

References 24 publications

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“…In addition, changes in the regulation of the HPA axis could be followed. Gotovac et al 54 have shown in their longitudinal study on a similar group of PTSD patients initially increased cortisol concentrations and natural killer cell cytotoxicity. However, cortisol concentrations decreased with the passing of time after a traumatic experience.…”

Section: Discussionmentioning

confidence: 99%

Oxidative status and the severity of clinical symptoms in patients with post-traumatic stress disorder

et al. 2014

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Background: The aim of this study was to measure the parameters of oxidative stress in the blood of patients with post-traumatic stress disorder. Methods: The study included 80 male war veterans who participated actively in the Homeland war in Croatia. Volunteers were divided into two groups: 50 veterans diagnosed with post-traumatic stress disorder and 30 without diagnosis. The self-assessment Hospital Anxiety and Depression Scale and the Beck Depression Inventory were used to detect the severity of depression and anxiety in the post-traumatic stress disorder patients. Catalytic concentrations of superoxide dismutase and glutathione peroxidase in erythrocytes and the concentration of malondialdehyde in serum were measured spectrophotometrically. Results: Although the catalytic concentrations of erythrocyte superoxide dismutase and erythrocyte glutathione peroxidase were within the reference range for both groups, the values obtained for the post-traumatic stress disorder group were significantly lower (P < 0.001). For serum malondialdehyde concentrations, no statistically significant differences between the groups were found. Conclusions: Lower catalytic concentrations of erythrocyte superoxide dismutase and erythrocyte glutathione peroxidase in patients with post-traumatic stress disorder may indicate a weaker response to oxidative stress due to impaired enzyme activity and/or decreased synthesis. Conversely, no significant changes in serum malondialdehyde concentrations suggest a compensated balance and adaptive response to (oxidative) stress.

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Section: Discussionmentioning

confidence: 99%

Oxidative status and the severity of clinical symptoms in patients with post-traumatic stress disorder

et al. 2014

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“…[30][31][32] Flow cytometric determination of GR expression in lymphocyte subpopulations even revealed a lower GR expression in all lymphocyte subsets from PTSD patients compared to healthy individuals. 33 To get an indication of GR function in the immune system, the capacity of glucocorticoids to inhibit immune responses in vitro 32,34 as well as in vivo dexamethasone (DEX)-induced changes in leukocyte GR binding 30,31 have been measured in PTSD.…”

Section: Introductionmentioning

confidence: 99%

Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

et al. 2007

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Post-traumatic stress disorder (PTSD) is associated with a dysregulation of the hypothalamus-pituitary-adrenal axis (HPA axis). In addition, there is evidence for altered glucocorticoid receptor (GR) expression and function in peripheral blood mononuclear cells. The aim of the present study was to differentiate between the effect of trauma exposure and PTSD on leukocyte GR expression and glucocorticoid immune regulation. Leukocyte GR binding characteristics and glucocorticoid sensitivity of immune activity, determined as the effect of dexamethasone (DEX) on in vitro cytokine release and T-cell proliferation, were compared between veterans with PTSD, traumatized veterans without PTSD and healthy controls. Leukocyte GR density was significantly lower in veterans with and without PTSD compared to healthy controls. DEX-induced inhibition of T-cell proliferation was significantly lower in PTSD compared to trauma and healthy controls. DEX-induced increase in lipopolysaccharidestimulated interleukin-10 was less pronounced in traumatized veterans with and without PTSD compared to healthy controls. No group differences were observed in the effect of DEX on other cytokines or in baseline immune activity, except for lower tumor necrosis factor-a production in PTSD patients compared to healthy controls. The results suggest that trauma exposure is sufficient to induce changes in GR binding characteristics, whereas resistance of T-cell proliferation to DEX only occurs in PTSD. DEX resistance of in vitro immune activity was not a general phenomenon, but was restricted to specific immune functions.

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“…PTSD has been associated with low plasma cortisol and an increased sensitivity to glucocorticoids (Coupland et al, 2003;Goenjian et al, 1996;Gotovac et al, 2003;Rohleder et al, 2004;Stein et al, 1997b;Yehuda et al, 1995Yehuda et al, , 2004a. Changes in trace eyeblink conditioning following a pharmacological challenge with hydrocortisone could help evaluate glucocorticoid sensitivity of focal brain regions such as the hippocampus in PTSD.…”

Section: Introductionmentioning

confidence: 99%

Hydrocortisone Impairs Hippocampal-Dependent Trace Eyeblink Conditioning in Post-Traumatic Stress Disorder

Vythilingam

Lawley

Collin³

et al. 2005

Neuropsychopharmacol

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Trace eyeblink conditioning is a hippocampal-dependent associative learning task that could help evaluate hippocampal function in Posttraumatic stress disorder (PTSD). Since preclinical research has demonstrated that trace eyeblink conditioning can be pharmacologically manipulated by glucocorticoids, this task may shed light on glucocorticoid sensitivity in PTSD. This study assessed baseline and hydrocortisone-mediated changes in trace eyeblink conditioning in patients with PTSD and in healthy controls. A total of 12 patients with PTSD and 12 age-and sex-matched healthy controls participated in a trace eyeblink test 6 h following intravenous administration of 30 mg of hydrocortisone. Spontaneous blink rates were similar between PTSD patients and healthy controls. There was no significant difference in the mean conditioned response between PTSD subjects and healthy controls under placebo conditions. Following hydrocortisone administration, only the PTSD patients demonstrated a significant reduction in conditioned response in contrast to healthy subjects who did not demonstrate any change. Patients with PTSD had increased glucocorticoid sensitivity in the focal brain regions mediating trace eyeblink conditioning.

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Flow cytometric determination of glucocorticoid receptor (GCR) expression in lymphocyte subpopulations: lower quantity of GCR in patients with post-traumatic stress disorder (PTSD)

Cited by 83 publications

References 24 publications

Oxidative status and the severity of clinical symptoms in patients with post-traumatic stress disorder

Oxidative status and the severity of clinical symptoms in patients with post-traumatic stress disorder

Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

Hydrocortisone Impairs Hippocampal-Dependent Trace Eyeblink Conditioning in Post-Traumatic Stress Disorder

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