Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder.

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Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder. / Pace, Thaddeus W W; Wingenfeld, Katja; Schmidt, Iris; Meinlschmidt, Gunther; Hellhammer, Dirk H; Heim, Christine M.

in: BRAIN BEHAV IMMUN, Jahrgang 26, Nr. 1, 1, 2012, S. 13-17.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

APA

Pace, T. W. W., Wingenfeld, K., Schmidt, I., Meinlschmidt, G., Hellhammer, D. H., & Heim, C. M. (2012). Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder. BRAIN BEHAV IMMUN, 26(1), 13-17. [1]. http://www.ncbi.nlm.nih.gov/pubmed/21801830?dopt=Citation

Vancouver

Pace TWW, Wingenfeld K, Schmidt I, Meinlschmidt G, Hellhammer DH, Heim CM. Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder. BRAIN BEHAV IMMUN. 2012;26(1):13-17. 1.

Bibtex

@article{887f83fadb3c47c9a55758d2d58485c5,
title = "Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder.",
abstract = "In addition to neuroendocrine changes PTSD pathophysiology may also involve dysfunction of the innate immune inflammatory system. PTSD patients have been found to exhibit increased concentrations of circulating inflammatory markers such as C-reactive protein and interleukin-6, suggesting dysfunction of the innate immune inflammatory system. However, few studies have investigated molecular signaling pathways known to critically regulate inflammation. Additionally, the relationship between inflammatory function and immune cell glucocorticoid sensitivity has not been extensively explored in PTSD. Nuclear factor-?B (NF-?B) pathway activity was examined in peripheral blood mononuclear cells obtained from 12 women with childhood abuse-related PTSD and 24 healthy controls (ages 19-48) using DNA-binding ELISA. Glucocorticoid sensitivity of monocytes in whole blood was measured as the concentration of dexamethasone needed to suppress in vitro lipopolysaccharide-induced tumor necrosis factor-alpha production by 50% (DEX IC(50)). Women with PTSD displayed increased NF-?B pathway activity compared to controls (t [34]=2.45, p=0.02) that was positively correlated with PTSD severity (determined by PTSD symptom severity scale) (r(s)=0.39, p=0.02). Increased NF-?B pathway activity was associated with increased whole blood monocyte DEX IC(50) (i.e. decreased sensitivity of monocytes to glucocorticoids) across all participants (r=0.66, p",
keywords = "Adult, Humans, Female, Middle Aged, Psychiatric Status Rating Scales, Young Adult, Child, Depression/psychology, Hydrocortisone/blood, Signal Transduction/*physiology, Monocytes/metabolism, Adult Survivors of Child Abuse/*psychology, Child Abuse, Sexual/*psychology, Glucocorticoids/blood, NF-kappa B/metabolism/*physiology, Neural Pathways/*metabolism, Peripheral Nervous System/metabolism/*physiology, Stress Disorders, Post-Traumatic/etiology/physiopathology/*psychology, Adult, Humans, Female, Middle Aged, Psychiatric Status Rating Scales, Young Adult, Child, Depression/psychology, Hydrocortisone/blood, Signal Transduction/*physiology, Monocytes/metabolism, Adult Survivors of Child Abuse/*psychology, Child Abuse, Sexual/*psychology, Glucocorticoids/blood, NF-kappa B/metabolism/*physiology, Neural Pathways/*metabolism, Peripheral Nervous System/metabolism/*physiology, Stress Disorders, Post-Traumatic/etiology/physiopathology/*psychology",
author = "Pace, {Thaddeus W W} and Katja Wingenfeld and Iris Schmidt and Gunther Meinlschmidt and Hellhammer, {Dirk H} and Heim, {Christine M}",
year = "2012",
language = "English",
volume = "26",
pages = "13--17",
journal = "BRAIN BEHAV IMMUN",
issn = "0889-1591",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder.

AU - Pace, Thaddeus W W

AU - Wingenfeld, Katja

AU - Schmidt, Iris

AU - Meinlschmidt, Gunther

AU - Hellhammer, Dirk H

AU - Heim, Christine M

PY - 2012

Y1 - 2012

N2 - In addition to neuroendocrine changes PTSD pathophysiology may also involve dysfunction of the innate immune inflammatory system. PTSD patients have been found to exhibit increased concentrations of circulating inflammatory markers such as C-reactive protein and interleukin-6, suggesting dysfunction of the innate immune inflammatory system. However, few studies have investigated molecular signaling pathways known to critically regulate inflammation. Additionally, the relationship between inflammatory function and immune cell glucocorticoid sensitivity has not been extensively explored in PTSD. Nuclear factor-?B (NF-?B) pathway activity was examined in peripheral blood mononuclear cells obtained from 12 women with childhood abuse-related PTSD and 24 healthy controls (ages 19-48) using DNA-binding ELISA. Glucocorticoid sensitivity of monocytes in whole blood was measured as the concentration of dexamethasone needed to suppress in vitro lipopolysaccharide-induced tumor necrosis factor-alpha production by 50% (DEX IC(50)). Women with PTSD displayed increased NF-?B pathway activity compared to controls (t [34]=2.45, p=0.02) that was positively correlated with PTSD severity (determined by PTSD symptom severity scale) (r(s)=0.39, p=0.02). Increased NF-?B pathway activity was associated with increased whole blood monocyte DEX IC(50) (i.e. decreased sensitivity of monocytes to glucocorticoids) across all participants (r=0.66, p

AB - In addition to neuroendocrine changes PTSD pathophysiology may also involve dysfunction of the innate immune inflammatory system. PTSD patients have been found to exhibit increased concentrations of circulating inflammatory markers such as C-reactive protein and interleukin-6, suggesting dysfunction of the innate immune inflammatory system. However, few studies have investigated molecular signaling pathways known to critically regulate inflammation. Additionally, the relationship between inflammatory function and immune cell glucocorticoid sensitivity has not been extensively explored in PTSD. Nuclear factor-?B (NF-?B) pathway activity was examined in peripheral blood mononuclear cells obtained from 12 women with childhood abuse-related PTSD and 24 healthy controls (ages 19-48) using DNA-binding ELISA. Glucocorticoid sensitivity of monocytes in whole blood was measured as the concentration of dexamethasone needed to suppress in vitro lipopolysaccharide-induced tumor necrosis factor-alpha production by 50% (DEX IC(50)). Women with PTSD displayed increased NF-?B pathway activity compared to controls (t [34]=2.45, p=0.02) that was positively correlated with PTSD severity (determined by PTSD symptom severity scale) (r(s)=0.39, p=0.02). Increased NF-?B pathway activity was associated with increased whole blood monocyte DEX IC(50) (i.e. decreased sensitivity of monocytes to glucocorticoids) across all participants (r=0.66, p

KW - Adult

KW - Humans

KW - Female

KW - Middle Aged

KW - Psychiatric Status Rating Scales

KW - Young Adult

KW - Child

KW - Depression/psychology

KW - Hydrocortisone/blood

KW - Signal Transduction/physiology

KW - Monocytes/metabolism

KW - Adult Survivors of Child Abuse/psychology

KW - Child Abuse, Sexual/psychology

KW - Glucocorticoids/blood

KW - NF-kappa B/metabolism/physiology

KW - Neural Pathways/metabolism

KW - Peripheral Nervous System/metabolism/physiology

KW - Stress Disorders, Post-Traumatic/etiology/physiopathology/psychology

KW - Adult

KW - Humans

KW - Female

KW - Middle Aged

KW - Psychiatric Status Rating Scales

KW - Young Adult

KW - Child

KW - Depression/psychology

KW - Hydrocortisone/blood

KW - Signal Transduction/physiology

KW - Monocytes/metabolism

KW - Adult Survivors of Child Abuse/psychology

KW - Child Abuse, Sexual/psychology

KW - Glucocorticoids/blood

KW - NF-kappa B/metabolism/physiology

KW - Neural Pathways/metabolism

KW - Peripheral Nervous System/metabolism/physiology

KW - Stress Disorders, Post-Traumatic/etiology/physiopathology/psychology

M3 - SCORING: Journal article

VL - 26

SP - 13

EP - 17

JO - BRAIN BEHAV IMMUN

JF - BRAIN BEHAV IMMUN

SN - 0889-1591

IS - 1

M1 - 1

ER -