Résumé
Recent findings suggest the existence of a chronic low-grade inflammation in suicidal behavior. Postmortem studies demonstrated associations between suicide and inflammatory cytokines in the orbitofrontal cortex, a brain region involved in suicidal vulnerability. Also, microgliosis and monocyte–macrophage system activation may be a useful marker of suicide neurobiology. Kynurenine may influence inflammatory processes, and related molecular pathways may be involved in SB pathophysiology. Studies associated inflammatory markers with several indicators of suicidal vulnerability: serotonin dysfunction, impulsivity, and childhood trauma. Furthermore, the perception of threat that leads suicidal individuals to contemplate suicide may activate biological stress responses, including inflammatory responses. This new line of evidence involving inflammation along the development of a suicidal vulnerability should foster translational projects aimed at identifying potential biomarkers of suicidal behavior. These researches might lead to new biomarkers and novel directions for therapeutic strategies.