Protein level in Bronchoalveolar lavage fluid (BALF) of rats was measured using Bradford Protein Assay Kit (B-Pak) from OZ Biosciences.
This article demonstrate the capacity of the Bradford Protein Assay Kit from OZ Biosciences to efficiently measure the total protein concentration in BALF of mice lung.article reference: J Neurotrauma. 2013 Aug 12.
Traumatic brain injury in rats induces lung injury and systemic immune suppression.
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.
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.
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