The cytokine response to human traumatic brain injury: temporal profiles and evidence for cerebral parenchymal production.

摘要: The role of neuroinflammation is increasingly being recognised in a diverse range cerebral pathologies, including traumatic brain injury (TBI). We used microdialysis and paired arterial jugular bulb plasma sampling to characterise the production 42 cytokines after severe TBI 12 patients over 5 days. compared two perfusates six patients: central nervous system perfusion fluid 3.5% human albumin solution (HAS); HAS has superior recovery (95.8 versus 83.3%), relative 18 (versus 8 42), qualitatively profile. All were recovered from brain. Sixteen showed stereotyped temporal peak, at least twice median value for that cytokine monitoring period; day 1: tumour necrosis factor, interleukin (IL)7, IL8, macrophage inflammatory protein (MIP)1α, soluble CD40 ligand, GRO, IL1β, platelet derived growth factor (PDGF)-AA, MIP1β, RANTES; 2: IL1 receptor antagonist (ra). IL6, granulocyte-colony stimulating (G-CSF), chemokine CXC motif ligand 10 (IP10); days 4 5: IL12p70, IL10. Brain extracellular concentrations significantly higher than 19 cytokines: basic fibroblast (FGF2), G-CSF, IL1α, IL1ra, IL3, IL10, IL12p40, IP10, monocyte chemotactic (MCP)1, MCP3, MIP1α, PDGF-AA, transforming (TGF)α vascular endothelial factor. No clear arterio-jugular venous gradients apparent. These data provide evidence these show pattern TBI.