Differential immunoresponses following experimental traumatic brain injury, bone fracture and "two-hit"-combined neurotrauma

Inflamm Res. 2007 Aug;56(8):318-23. doi: 10.1007/s00011-007-6141-3.

Abstract

Objective and design: 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).

Materials and methods: 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.

Results: 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).

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Injuries / immunology*
  • Interleukin-10 / blood
  • Interleukin-6 / blood
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Tumor Necrosis Factor, Type I / blood
  • Tibial Fractures / immunology*
  • Whole-Body Irradiation

Substances

  • Interleukin-6
  • Receptors, Tumor Necrosis Factor, Type I
  • Interleukin-10