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Disease Markers
Volume 30 (2011), Issue 2-3, Pages 123-132

Transcriptional Control of Monocyte Gene Expression in Post-Traumatic Stress Disorder

Aoife O’Donovan,1,2,3 Bing Sun,1,2,4 Steve Cole,5 Hans Rempel,1,2 Maryann Lenoci,1,2,3 Lynn Pulliam,1,2,4 and Thomas Neylan1,2,3

1Veteran’s Affairs Medical Center, San Francisco, CA, USA
2Northern California Institute for Research and Education, San Francisco, CA, USA
3Department of Psychiatry, University of California, San Francisco, CA, USA
4Department of Laboratory Medicine, University of California, San Francisco, CA, USA
5Department of Medicine, University of California, Los Angeles, CA, USA

Received 14 April 2011; Accepted 14 April 2011

Copyright © 2011 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Post-traumatic stress disorder (PTSD) confers an increased risk for disorders with an inflammatory etiology. PTSD-related dysregulation of the sympathetic nervous system (SNS) and hypothalamic-pituitary adrenal (HPA) axis and associated alterations in inflammatory activity may contribute to this increased risk. However, little is known about convergent SNS, HPA and inflammatory signaling at the level of the immune cell transcriptome in PTSD. To explore such signaling, we examined the prevalence of specific transcription factor binding motifs in the promoter regions of differentially expressed genes in monocytes from individuals with PTSD and matched controls. Participants included 49 men (24 PTSD+ and 25 trauma-exposed controls) and 18 women (10 PTSD+ and 8 controls). Men with PTSD showed up-regulation of target genes for the NF-κB/Rel family of transcription factors, which convey inflammatory signals, up-regulation of target genes for CREB/ATF transcription factors, which convey adrenergic signals from the SNS, and down-regulation of target genes for the glucocorticoid receptor, which conveys glucocorticoid signals from the HPA axis. Women with PTSD also showed significant up-regulation of target genes for NF-κB and non-significant down-regulation of target genes for GR, but significant down-regulation of target genes for CREB/ATF. Altered transcriptional control of monocyte gene expression could contribute to exaggerated inflammatory activity in PTSD.