Journal
NEUROPHARMACOLOGY
Volume 62, Issue 2, Pages 663-673Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2011.02.027
Keywords
Posttraumatic stress disorder (PTSD); Depression; Stress; Immune; Cytokine; HPA axis
Categories
Funding
- VA (HSRD)
- DOD (BUMED, CDMRP) Research
- VA Center of Excellence for Stress and Mental Health
- NIMH [1 U01 MH092758-01]
- NIA [1 R01 AG030474-01A2]
- [HL58120 MD000220 (EXPORT/CRCHD)]
- [RR031980 (CTSA)]
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The biological underpinnings for participation of the immune system in the pathogenesis of Posttraumatic Stress Disorder (PTSD) include evidence for cross-talk between the stress and immune systems, as well as more recently discovered roles for immune system mediators in core behavioral functions such as adult neurogenesis, as well as in processes that underlay synaptic plasticity, such as learning and memory. This article reviews the expanding body of literature on immune system mediators in the periphery and the central nervous system (CNS) in chronic PTSD along with the evidence for increased peripheral inflammation, and excess morbidity and mortality. CNS inflammation has been implicated in the pathogenesis of depression. This literature is briefly reviewed, along with evidence for a possible role for CNS inflammation in PTSD symptoms, especially in individuals who have PTSD with co-morbid depression. Whether the immune system is involved in risk and resilience, or evolution of PTSD symptoms following a trauma event remains to be determined, although hypotheses have been advanced. This paper reviews the current evidence including the novel hypothesis that cellular immunity is implicated in PTSD risk and resilience. Potential research implications and directions are discussed. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'. Published by Elsevier Ltd.
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