Traumatic brain injury is not a major driver of early systemic neutrophil activation in polytrauma patients

Background Traumatic brain injury (TBI) induces local neuroinflammation and has been associated with systemic immune alterations. However, whether concomitant TBI provides an additional stimulus for early systemic neutrophil activation in severely injured polytrauma patients remains unclear. We investigated the association of TBI with circulating neutrophil abundance and surface receptor expression immediately after trauma. Methods In this prospective observational study, adult polytrauma patients with an Injury Severity Score (ISS) ≥ 16 were included. Peripheral blood was obtained immediately after admission to the trauma bay. Parameters on circulation leukocytes, as well neutrophil cell surface marker expression of CD10, CD11b, CD16, CD62L, and CD64 was quantified by an automated flow cytometer. Patients were compared according to the presence of TBI. Results Overall, 46 patients were included, with a median ISS of 34 and a mean age of 53.9 years. Admission leukocyte counts ( p = 0.183), neutrophil counts ( p = 0.256), and NLR ( p = 0.937) were comparable between patients with and without TBI. Likewise, no significant differences were observed in CD11b ( p = 0.751), CD16 ( p = 0.343), CD62L ( p = 0.883), CD10 ( p = 0.419), or CD64 expression ( p = 0.520). Furthermore, neutrophil surface marker expression did not differ across GCS categories and showed no significant association with the severity of cranial trauma. In addition, no association with later development of delirium was observed for the investigated markers. Conclusion Concomitant TBI was not associated higher systemic neutrophil activation in severely injured polytrauma patients at hospital admission. These findings suggest that the immediate peripheral neutrophil response may predominantly reflect the overall trauma burden rather than the presence of TBI or alternatively, TBI contributes to neutrophil activation but at a later timepoint, as the brain-blood barrier is intact at the point of admission. Longitudinal studies are required to determine whether TBI-specific alterations emerge during later phases after injury.