Inflammation in Posttraumatic Stress Disorder: Dysregulation or Recalibration?


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Abstract

Despite ample experimental data indicating a role of inflammatory mediators in the behavioral and neurobiological manifestations elicited by exposure to physical and psychologic stressors, causative associations between systemic low-grade inflammation and central nervous system inflammatory processes in posttraumatic stress disorder (PTSD) patients remain largely conceptual. As in other stress-related disorders, pro-inflammatory activity may play an equivocal role in PTSD pathophysiology, one that renders indiscriminate employment of anti-inflammatory agents of questionable relevance. In fact, as several pieces of preclinical and clinical research convergingly suggest, timely and targeted potentiation rather than inhibition of inflammatory responses may actually be beneficial in patients who are characterized by suppressed microglia function in the face of systemic low-grade inflammation. The deleterious impact of chronic stress-associated inflammation on the systemic level may, thus, need to be held in context with the - often not readily apparent - adaptive payoffs of low-grade inflammation at the tissue level.

About the authors

Kostas Patas

Department of Biopathology and Laboratory Medicine, Eginition University Hospital

Email: info@benthamscience.net

Dewleen Baker

Department of Psychiatry, University of California

Email: info@benthamscience.net

George Chrousos

Medical School, Aghia Sophia Children's Hospital, University Research Institute of Maternal and Child Health and Precision Medicine and UNESCO Chair on Adolescent Health Care, National and Kapodistrian University of Athens

Email: info@benthamscience.net

Agorastos Agorastos

VA Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System

Author for correspondence.
Email: info@benthamscience.net

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