BACKGROUND: Borderline personality disorder (BPD) and eating disorders (ED) are both disorders with emotional dysregulation that may share some similar biological underpinnings, leading to oxidative/inflammatory alterations. Unfortunately, to date, no studies have assessed the relationship between clinical features, inflammatory alterations and childhood trauma across these disorders. Our aim was to identify the potential common and disorder-specific inflammatory pathways and examine possible associations between these dysregulated pathways and the clinical features. METHODS: We studied a sample of 108 women (m = 27.17 years; sd = 7.64), divided into four groups: 23 patients with a restrictive ED (ED-R), 23 patients with a bingeeating/ purging ED (ED-P) and 26 patients with BPD; whereas the control group included 23 healthy subjects. Several inflammatory/oxidative parameters: tumor necrosis factor alpha (TNFα), Thiobarbituric Acid Reactive Substances (TBARS), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), p38 mitogenactivated protein kinases, ERK mitogen-activated protein kinases and c-Jun NH2- terminal kinase (JNK), and some antiinflammatory antioxidant elements: glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), Kelch-like ECHassociated protein (Keap1) were determined in plasma or peripheral blood mononuclear cells. Furthermore, clinical, impulsivity, trauma and eating behavior questionnaires were administered. RESULTS: Three main inflammatory/oxidative components were extracted using principal component analysis (59.19 % of biomarker variance explained). Disorder-specific dysfunction in the inflammatory and oxidative pathways in patients with BPD and ED were revealed by means of relationships with specific principal components (p < .01). BPD patients showed higher levels of a component featured by elevated levels of JNK and lower of GPx and SOD. ED-R and impulsivity were associated with a component featured by the activation of ERK and negative influence of Keap1. The component featured by the suppression of catalase and COX2 was associated with both ED subtypes and trauma exposure. CONCLUSION: Several risk factors such as trauma, impulsivity and eating disorder symptoms were transdiagnostically associated with some inflammatory alterations regardless of diagnosis. These findings suggest that the clinical profile comprising trauma exposure and an emotional dysregulation disorder might constitute a specific endophenotype highly linked with inflammatory alterations.