The proteomic and metabolomic signatures of isolated and polytrauma traumatic brain injury

• Published in: The American journal of surgery Vol. 226; no. 6; pp. 790 - 797
• Main Authors: Cralley, Alexis L., Erickson, Chris, Schaid, Terry R., Hallas, William, Thielen, Otto, Mitra, Sanchayita, Stafford, Preston, Hom, Patrick, Silliman, Christopher, Cohen, Mitchell J., Moore, Ernest E., D'Alessandro, Angelo, Hansen, Kirk C.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2023; Elsevier Limited
• Subjects: Apolipoproteins; Bile acids; Blood platelets; Blood-brain barrier; Brain; Brain research; Coagulation; Customization; Dehydrogenases; Glycolysis; Head injuries; Hemorrhagic shock; Metabolism; Metabolites; Metabolomics; Mortality; Patients; Peptides; Polytrauma; Precision medicine; Proteins; Proteomics; Trauma; Trauma centers; Trauma inflammatory milieu; Traumatic brain injury; Variables; Trauma inflammatory milieu; Traumatic brain injury; Polytrauma; Proteomics
• ISSN: 0002-9610; 1879-1883
• DOI: 10.1016/j.amjsurg.2023.07.040

The interactions of polytrauma, shock, and traumatic brain injury (TBI) on thromboinflammatory responses remain unclear and warrant investigation as we strive towards personalized medicine in trauma. We hypothesized that comprehensive omics characterization of plasma would identify unique metabolic and thromboinflammatory pathways following TBI. Patients were categorized as TBI vs Non-TBI, and stratified into Polytrauma or minimally injured. Discovery ‘omics was employed to quantify the top differently expressed proteins and metabolites of TBI and Non-TBI patient groups. TBI compared to Non-TBI showed gene enrichment in coagulation/complement cascades and neuronal markers. TBI was associated with elevation in glycolytic metabolites and conjugated bile acids. Division into isolated TBI vs polytrauma showed further distinction of proteomic and metabolomic signatures. Identified mediators involving in neural inflammation, blood brain barrier disruption, and bile acid building leading to TBI associated coagulopathy offer suggestions for follow up mechanistic studies to target personalized interventions. •Omic techniques accelerate understanding of the molecular pathways triggered by TBI.•TBI bile acid accumulation may contribute to coagulopathy.•Key markers blood brain barrier disruption are detected in early plasma samples in TBI patients.