Abstract
Post-traumatic stress disorder (PTSD) is associated with inflammatory immune activity, including higher levels of pro-inflammatory cytokines. These inflammatory activities, together with other pathophysiologic mechanisms, link PTSD to somatic diseases like cardiovascular disease and diabetes. The inflammatory activities in PTSD can be moderated by various cellular and molecular processes, ranging from changes in a number of receptors to cross-talking with immune pathway components on the transcription factor level. In addition, age, gender, personality, genetics, smaller hippocampal size, social support, and experiences prior to the traumatic event are important risk and resilience factors to consider in the development of PTSD, which can often be linked directly or indirectly to inflammatory markers.