Citation

Vermeij JD, Aslami H, Fluiter K, Roelofs JJ, van den Bergh WM, Juffermans NP, Schultz MJ, van der Sluijs K, van de Beek D, van Westerloo DJ. J. Neurotrauma 2013; 30(24): 2073-2079.

Affiliation

Academic Medical Center, Neurology, Amsterdam, Netherlands ; j.d.vermeij@amc.uva.nl.

Copyright

(Copyright © 2013, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2013.3060

PMID

23937270

Abstract

Traumatic brain injury (TBI) is frequently complicated by acute lung injury, which is predictive for poor outcome. However, it is unclear whether lung injury develops independently or as a result of mechanical ventilation after TBI. Furthermore TBI is strongly associated with the development of pneumonia suggesting a specific vulnerability for the development of nosocomial infections in the lung after TBI. In this study we evaluated whether indeed pulmonary injury and immune suppression develop spontaneously in an animal model of mild TBI. TBI was induced in male PVG rats by closed head trauma using a weight drop device. Subsequently we evaluated the effects of this on the lungs as well as on the excitability of the systemic immune system. Finally, we performed an experiment in which TBI was followed by induction of pneumonitis and evaluated whether TBI impacts on the severity of subsequent pneumonitis induced by intratracheal instillation of heat killed Staphylococcus aureus. Mild TBI resulted in significant lung injury as evidenced by pulmonary edema, protein leakage to the alveolar compartment and increased concentrations of interleukin 1 and 6 in broncho alveolar lavage fluid (all p<0.05 versus sham treated animals). Furthermore, after TBI the release of TNF alpha was decreased when whole blood was stimulated ex vivo (p<0.05 TBI versus sham) indicating systemic immune suppression. When TBI was followed by pneumonitis the severity of subsequent pneumonitis was not different in rats previously subjected to TBI or sham treatment (p>0.05) suggesting that systemic immune suppression is not translated towards the pulmonary compartment in this specific model. We here show that during mild experimental TBI acute pulmonary injury as well as a decrease in the excitability of the systemic immune system can be observed.

Language: en