期刊
INFLAMMATION RESEARCH
卷 56, 期 8, 页码 318-323出版社
SPRINGER BASEL AG
DOI: 10.1007/s00011-007-6141-3
关键词
cytokines; traumatic brain injury; tibia fracture; combined neurotrauma; inflammatory response
Cytokine-mediated immunoresponses are consequences of isolated traumatic brain injury (TBI) and muskuloskeletal trauma but little is known when both impacts occur simulanteously in combined neurotrauma (CNT), i. e. TBI + muskuloskeletal trauma (bone fracture). A two-hit-experimental model of CNT (TBI + tibia fracture) was used to investigate circulating cytokine interleukin-1-beta, -6, -10 and sTNF-R1 concentrations following peripheral bone fracture only, TBI only and CNT. Blood samples were drawn at 30 min, 6 h, 24 h, 48 h, and 7 days following trauma and circulating cytokine concentrations were determined via immunoassay. Circulating cytokines were increased after trauma (p < 0.001 vs. controls), but peaked at different time points. sTNF R1 peaked first at 30 min, followed by IL-6 at 6 h after trauma. IL-10 levels were highest at 24 h, and those for IL-1beta at 48 h after trauma. Circulating IL-6 and IL-10 levels were highest in CNT at 8/10 time points studied (p < 0.001). Circulating cytokine IL-1-beta, -6, -10 and sTNF-R1 concentrations are increased after trauma (TBI, fracture and CNT) but peak at different time points. Pronounced IL-6 and IL-10 responses after CNT may contribute to the increased susceptibility for complications in CNT versus monotrauma.
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