Inflammation and traumatic stress

Hiroaki Hori, Yuko Hakamata

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Mounting evidence indicates that early-life adversity can cause a long-lasting increase in circulating proinflammatory markers, such as interleukin-6 and C-reactive protein. Stress-related psychiatric disorders including posttraumatic stress disorder (PTSD) have been associated with early adversity and increased inflammation. Therefore, it is suggested that inflammation may represent an important route through which early adversity increases the risk of developing PTSD in later life. While the exact mechanism underlying the association between traumatic stress and inflammation is unclear, increased inflammation can be involved in the etiology of PTSD as part of the stress response, in concert with the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Future studies are needed to clarify whether traumatic stress-associated inflammation is also present in the brain as well as in the periphery.

Original languageEnglish
Title of host publicationStress
Subtitle of host publicationImmunology and Inflammation: Handbook of Stress Series Volume 5
PublisherElsevier
Pages65-75
Number of pages11
Volume5
ISBN (Electronic)9780128175583
ISBN (Print)9780128175590
DOIs
StatePublished - 2023/01/01

Keywords

  • C-reactive protein (CRP)
  • Early-life adversity
  • Hypothalamic-pituitary-adrenal (HPA) axis
  • Inflammation
  • Interleukin-6 (IL-6)
  • Major depressive disorder (MDD)
  • Posttraumatic stress disorder (PTSD)
  • Stress

ASJC Scopus subject areas

  • General Neuroscience

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