*2.2. Eligibility Criteria*

Studies included in the current review were first screened such that they were original research articles using a human cohort, with a target population of PTSD that also explored the alteration in inflammatory state. The following records were to be excluded as part of the screening process: (1) records that are not original research including review papers, conference abstracts, short communications, or commentaries, (2) studies that used animal models, in vitro models, or post-mortem studies, (3) records that were not in English language, or (4) study designs that did not investigate inflammation in a target population of PTSD. After the screening process, the eligibility of the remaining articles was assessed using a full-text review. Articles that met the following criteria were further excluded: (1) studies that investigated PTSD with other comorbid disorders, diseases, or medical conditions (i.e., bipolar disorder, major depressive disorder, cardiovascular disease, myocardial infarction, etc.), or (2) studies that performed clinical trials or other forms of intervention as part of the study design. In addition, studies that investigated the inflammatory state in PTSD from a pediatric sample population were excluded, as well as target population of childhood onset trauma, as previous literature noted that the time lag between the time of trauma and time of assessment or sampling may influence the degree of alteration in inflammatory cytokine levels [24].

## *2.3. Inflammatory Markers of Interest*

For the current review, a select number of inflammatory markers that were previously described as potential biomarkers of PTSD [26,27] were targeted as methods of assessment for inflammation. Studies that investigated the alterations in these selected inflammatory markers were considered eligible, including levels of proinflammatory and anti-inflammatory cytokines. Specifically, cytokines that are most prevalently observed as being altered in relation to PTSD were selected as follows: serum proinflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)- α, and interferon (IFN)-γ as well as C-reactive protein (CRP) which is influenced by proinflammatory cytokines [28], serum anti-inflammatory cytokines IL-4 and IL-10 [29], and PTSD- and oxidative stress-related genes including the brain-derived neurotrophic factor (*BDNF*), arachidonate 12-lipoxygenase (*ALOX12*), arachidonate 15-lipoxygenase (*ALOX15*), and retinoic acid orphan receptor alpha (*RORA*) [30]. Neuroimaging-based studies were also included such as MRI and PET, along with markers of inflammation to examine the moderating role of specific inflammatory markers in the alteration of the brain.
