PTSD and inflammation

Abstract

While posttraumatic stress disorder (PTSD) is diagnosed based on traditional psychobehavioral symptoms such as re-experiencing (or intrusion), accumulated evidence indicates a link between this disorder and alterations in the immune/inflammatory system. Epidemiological studies have shown that individuals with PTSD have significantly increased rates of physical comorbidities where immune dysregulation is involved, such as metabolic syndrome, atherosclerotic cardiovascular disease, and autoimmune diseases. In line with this, a number of blood biomarker studies have demonstrated that compared to healthy controls, individuals with PTSD show significantly elevated levels of proinflammatory markers such as interleukin-1β, interleukin-6, tumor necrosis factor-α, and C-reactive protein. Moreover, various lines of animal and human research have suggested that inflammation is not only associated with PTSD but can play an important role in its pathogenesis and pathophysiology. In this review, I first summarize evidence suggestive of increased inflammation in PTSD. Findings that suggest possible mechanisms of inflammation in this disorder are then examined in terms of two different (yet interrelated) perspectives: putative causes of increased proinflammatory activities and potential consequences that inflammation generates. Given that there is currently a dearth of treatment options for PTSD, possibilities of novel therapeutic strategies targeting inflammation are also discussed. Despite the growing attention given to the inflammatory pathology of PTSD, there remains much to be clarified, including more detailed mechanisms of inflammation, potential usefulness of inflammatory biomarkers as diagnostic and prognostic markers, and efficacy of new treatment approaches targeting inflammation.