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Trauma patients with type O blood exhibit unique multiomics signature with decreased lectin pathway of complement
Benjamin W Stocker1, Ian S LaCroix, Christopher Erickson
1From the Department of Surgery (B.W.S., L.T.G., B.J.R., O.T., W.H., S.M., E.E.M., C.C.S., M.J.C.), and Department of Biochemistry and Molecular Genetics (I.S.L., C.E., K.H., A.D.), School of Medicine, University of Colorado Anschutz Medical Campus, Aurora; Department of Surgery (E.E.M.), Ernest E Moore Shock Trauma Center, Denver Health Medical Center; Vitalant Research Institute (C.C.S.), Denver; and Department of Pediatrics (C.C.S.), School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Background:
Patients with type O blood may have an increased risk of hemorrhagic complications because of lower baseline levels of von Willebrand factor and factor VIII, but the transition to a mortality difference in trauma is less clear. We hypothesized that type O trauma patients will have differential proteomic and metabolomic signatures in response to trauma beyond von Willebrand factor and factor VIII alone.
Methods:
Patients meeting the highest level of trauma activation criteria were prospectively enrolled. Blood samples were collected upon arrival to the emergency department. Proteomic and metabolomic (multiomics) analyses of these samples were performed using liquid chromatography-mass spectrometry. Demographic, clinical, and multiomics data were compared between patients with type O blood versus all other patients.
Results:
There were 288 patients with multiomics data; 146 (51%) had type O blood. Demographics, injury patterns, and initial vital signs and laboratory measurements were not different between groups. Type O patients had increased lengths of stay (7 vs. 6 days, p = 0.041) and a trend toward decreased mortality secondary to traumatic brain injury compared with other causes (traumatic brain injury, 44.4% vs. 87.5%; p = 0.055). Type O patients had decreased levels of mannose-binding lectin and mannose-binding lectin-associated serine proteases 1 and 2, which are required for the initiation of the lectin pathway of complement activation. Type O patients also had metabolite differences signifying energy metabolism and mitochondrial dysfunction.
Conclusion:
Blood type O patients have a unique multiomics signature, including decreased levels of proteins required to activate the lectin complement pathway. This may lead to overall decreased levels of complement activation and decreased systemic inflammation in the acute phase, possibly leading to a survival advantage, especially in traumatic brain injury. However, this may later impair healing. Future work will need to confirm these associations, and animal studies are needed to test therapeutic targets.
Level Of Evidence:
Prognostic and Epidemiological; Level IV.
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