Borderline personality disorder and aggressive behavior: A study based on the DSM-5 alternative model.

INTRODUCTION: Unplanned reactive aggressive acts are a clinical feature of particular interest in patients with borderline personality disorder (BPD). The early identification of personality traits correlated to aggressive behavior is certainly desirable in BDP populations. This study analyzes a clinical sample of 122 adult outpatients with BPD referred to Adult Mental Health Services of the Department of Mental Health of Bologna, in Italy. METHODS: The study examines the relationship with personality facets of the DSM-5 alternative model for personality disorders (AMPD), Personality Inventory for DSM (PID-5), with respect to the four main components of aggression measured by the Aggression Questionnaire (AQ): hostility, anger, verbal and physical aggression. Using robust regression models, the relationships between PID-5 facets and domains and the aggression components under consideration were identified. RESULTS: Verbal and physical aggression in our sample of BPD outpatients is mainly associated to PID-5 antagonism domain. Physically aggressive behavior is also related to callousness facet. CONCLUSIONS: The traits most consistently associated with aggression were the domain of Antagonism and the facet of Hostility. The study findings highlight the need for clinicians working with individuals with BPD to pay particular attention to traits of hostility, callousness, and hostility to understand aggression.

GPBAR1 Functions as Gatekeeper for Liver NKT Cells and provides Counterregulatory Signals in Mouse Models of Immune-Mediated Hepatitis.

BACKGROUND & AIMS: GPBAR1, also known as TGR5, is a G protein-coupled receptor activated by bile acids. Hepatic innate immune cells are involved in the immunopathogenesis of human liver diseases and in several murine hepatitis models. Here, by using genetic and pharmacological approaches, we provide evidence that GPBAR1 ligation attenuates the inflammation in rodent models of hepatitis. MATERIAL AND METHODS: Hepatitis was induced by concanavalin A (Con A) or α-galactosyl-ceramide (α-GalCer). 6b-Ethyl-3a,7b-dihydroxy-5b-cholan-24-ol (BAR501), a selective agonist of GPBAR1, was administrated by o.s. RESULTS: In the mouse models of hepatitis, the genetic ablation of Gpabar1 worsened the severity of liver injury and resulted in a type I NKT cells phenotype that was biased toward a NKT1, a proinflammatory, IFN-γ producing, NKT cells subtype. Further on, NKT cells from GPBAR1-/- mice were sufficient to cause a severe hepatitis when transferred to naïve mice. In contrast, GPBAR1 agonism rescued wild-type mice from acute liver damage and redirects the NKT cells polarization toward a NKT10, a regulatory, IL-10 secreting, type I NKT cell subset. In addition, GPBAR1 agonism significantly expanded the subset of IL-10 secreting type II NKT cells. RNAseq analysis of both NKT cells type confirmed that IL-10 is a major target for GPABR1. Accordingly, IL-10 gene ablation abrogated protection afforded by GPBAR1 agonism in the Con A model. CONCLUSION: Present results illustrate a role for GPBAR1 in regulating liver NKT ecology. Because NKT cells are an essential component of liver immune system, our data provide a compelling evidence for a GPBAR1-IL-10 axis in regulating of liver immunity.