Abstract
Background. The molecular mechanisms of the immune response after polytrauma are highly complex and far from fully understood. In this paper, we characterize a new standardized polytrauma model in rats based on the early molecular inflammatory and apoptotic response. Methods. Male Wistar rats (250 g, 6–10/group) were anesthetized and exposed to chest trauma (ChT), closed head injury (CHI), or Tib/Fib fracture including a soft tissue trauma (Fx + STT) or to the following combination of injuries: (1) ChT; (2) ChT + Fx + STT; (3) ChT + CHI; (4) CHI; (5) polytrauma (PT = ChT + CHI + Fx + STT). Sham-operated rats served as negative controls. The inflammatory response was quantified at 2 hours and 4 hours after trauma by analysis of “key” inflammatory mediators, including selected cytokines and complement components, in serum and bronchoalveolar (BAL) fluid samples. Results. Polytraumatized (PT) rats showed a significant systemic and intrapulmonary release of cytokines, chemokines, and complement anaphylatoxins, compared to rats with isolated injuries or selected combinations of injuries. Conclusion. This new rat model appears to closely mimic the early immunological response of polytrauma observed in humans and may provide a valid basis for evaluation of the complex pathophysiology and future therapeutic immune modulatory approaches in experimental polytrauma.
Highlights
Trauma is still one of the leading causes of death among people aged 45 and younger
As a consequence of the injury severity and the immune status of the patients, the posttraumatic inflammatory response often results in an overindulging and uncontrolled activation of the complement system with an increased release of proinflammatory mediators [6] often resulting in multiple organ dysfunction and death
We describe a new polytrauma model in rats and characterize the early systemic and local inflammatory response accompanied by a rapid activation of the complement system similar to that seen in humans
Summary
Trauma is still one of the leading causes of death among people aged 45 and younger. The annual economic burden of direct and indirect costs in Germany alone is estimated to be around 40 billion Euros annually [1]. As a consequence of the injury severity and the immune status of the patients, the posttraumatic inflammatory response often results in an overindulging and uncontrolled activation of the complement system with an increased release of proinflammatory mediators [6] often resulting in multiple organ dysfunction and death. This new rat model appears to closely mimic the early immunological response of polytrauma observed in humans and may provide a valid basis for evaluation of the complex pathophysiology and future therapeutic immune modulatory approaches in experimental polytrauma
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