Editorial: Translational insights into mechanisms and therapy of organ dysfunction in sepsis and trauma

Abstract

Multiple organ dysfunction or even failure after sepsis or trauma is due to a dysregulated host response. Currently, besides (surgical) source control (e.g., control of bleeding or drainage of abscesses) and administration of antimicrobial drugs, therapeutic approaches are limited to supportive care. Advances in our understanding of the key pathophysiological pathways involved in the excessive inflammation triggered by trauma, sepsis and/or ischemia-reperfusion have had limited impact. The 28 article in this Research Topic focus on the molecular mechanisms behind (hyper) inflammation after sepsis or trauma, with special emphasis on preclinical and translational studies that target potential organ-protective and/or -resuscitative therapeutic strategies. Most studies report rodent models of trauma and elective surgery (three articles), non-microbial hyper-inflammation induced with endotoxin exposure (LPS; seven articles) and chemical pancreatitis (one article), and cecal ligation and puncture-induced sepsis (six articles). Additional papers summarize investigations of human material (six articles) or fully-resuscitated large animal models (two articles). These article are complimented by four reviews and a commentary