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

Pace, Thaddeus W. and Wingenfeld, Katja and Schmidt, Iris and Meinlschmidt, Gunther and Hellhammer, Dirk H. and Heim, Christine M.. (2012) Increased peripheral NF-kappaB pathway activity in women with childhood abuse-related posttraumatic stress disorder. Brain, behavior, and immunity, Vol. 26, H. 1. pp. 13-17.

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Official URL: http://edoc.unibas.ch/dok/A5848994

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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>0.001). These findings suggest that enhanced inflammatory system activity in participants with childhood abuse-related PTSD is observable at the level of NF-?B, and that in general decreased immune cell glucocorticoid sensitivity may contribute to increased NF-?B pathway activity. Enhanced inflammation may contribute to co-morbid somatic disease risk in persons with childhood abuse-related PTSD.
UniBasel Contributors:Meinlschmidt, Gunther and Hellhammer, Dirk H.
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Academic Press
ISSN:0889-1591
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:10 Oct 2014 09:19
Deposited On:14 Sep 2012 07:04

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