Inflammation in Posttraumatic Stress Disorder: Dysregulation or Recalibration?

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 sug- gest, 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 sy- stemic 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.

Thematic Selection: Stress and Stress-related Disorders Posttraumatic Stress Disorder (Part 2)

“…With their article, Antolasic et al review theoretical underpinnings of the involvement of BDNF and the Val66Met polymorphism in the development and persistence of intrusive and hypervigilance symptoms in PTSD [ 18 ]. Patas et al provide a novel take on immune and inflammatory findings in PTSD and offer some stimulating ideas on immune-based PTSD treatment alternatives [ 19 ]. The article by Sabé et al embodies a large scientometric analysis of 42,170 publications published between 1945 and 2022 to outline different aspects of clinical research in PTSD [ 20 ], while Lappas et al offer a detailed review of available literature on the effect of antidepressants on sleep in patients with PTSD [ 21 ].…”