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1. Traumatic brain injury (TBI) compromises innate immunity, leading to poor bacterial clearance in the lungs despite increased neutrophil counts.
2. Both mouse and pig models of TBI combined with bacterial lung infection demonstrate impaired bacterial clearance and altered neutrophil function.
3. Plasma and extracellular vesicles from human TBI patients induce neutrophil dysfunction characterized by excessive nondirectional movement, reduced reactive oxygen species production, and decreased phagocytosis.
4. Systemic factors post-TBI, including circulating plasma components, contribute to innate immune dysregulation increasing susceptibility to pulmonary bacterial infections.
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