The protective effect of the blood brain barrier from systemic cytokines in an animal femur fracture model

Abstract

Background: Previous studies of head trauma have shown profound release of cytokines in the brain. These changes were not expressed in peripheral tissues. The intent of this study was to take an animal model of femur fracture, monitor the expression of biochemical markers in the periphery, and compare this to their expression in the brain.

Methods: Rats were subjected to a weight-drop, femur fracture model, and then killed at various times. Samples of muscle, liver, serum, and brain were analyzed for concentrations of cytokines, and compared with controls.

Results: Statistically significant (p < 0.05) results from the study were found in the liver. Interleukin (IL)-2, IL-10, IL-11, and other acute phase reactants were elevated at 24 hours after injury, compared with in controls. Analysis of these cytokines in the brain showed no significant increase when compared with those of controls. Further analysis also demonstrated an increase in plasma C-reactive protein and leptin in the fracture group. These results differ from our previous brain trauma study, which demonstrated no increased expression of cytokines in liver or plasma.

Conclusions: This animal model of peripheral injury demonstrates that there is a significant rise in acute phase reactants in liver tissue and plasma within 24 hours after injury, without a corresponding rise in cytokine concentration in the brain. These results suggest that although the brain is potentially exposed to the biochemical response to injury, the brain parenchyma itself is protected from up-regulation of proinflammatory cytokines. Interestingly, this is the opposite effect seen in our isolated brain injury study.