@article{ref1,
title="Decreased secondary lesion growth and attenuated immune response after traumatic brain injury in Tlr2/4(-/-) mice",
journal="Frontiers in neurology",
year="2017",
author="Krieg, Sandro M. and Voigt, Florian and Knuefermann, Pascal and Kirschning, Carsten Jürgen and Plesnila, Nikolaus and Ringel, Florian",
volume="8",
number="",
pages="e455-e455",
abstract="Danger-associated molecular patterns are released by damaged cells and trigger neuroinflammation through activation of non-specific pattern recognition receptors, e.g., toll-like receptors (TLRs). Since the role of TLR2 and 4 after traumatic brain injury (TBI) is still unclear, we examined the outcome and the expression of pro-inflammatory mediators after experimental TBI in Tlr2/4(-/-) and wild-type (WT) mice. Tlr2/4(-/-) and WT mice were subjected to controlled cortical injury and contusion volume and brain edema formation were assessed 24 h thereafter. Expression of inflammatory markers in brain tissue was measured by quantitative PCR 15 min, 3 h, 6 h, 12 h, and 24 h after controlled cortical impact (CCI). Contusion volume was significantly attenuated in Tlr2/4(-/-) mice (29.7 ± 0.7 mm(3) as compared to 33.5 ± 0.8 mm(3) in WT; p < 0.05) after CCI while brain edema was not affected. Only interleukin (IL)-1β gene expression was increased after CCI in the Tlr2/4(-/-) relative to WT mice. Inducible nitric oxide synthetase, TNF, IL-6, and COX-2 were similar in injured WT and Tlr2/4(-/-) mice, while the increase in high-mobility group box 1 was attenuated at 6 h. TLR2 and 4 are consequently shown to potentially promote secondary brain injury after experimental CCI via neuroinflammation and may therefore represent a novel therapeutic target for the treatment of TBI.<p /> <p>Language: en</p>",
language="en",
issn="1664-2295",
doi="10.3389/fneur.2017.00455",
url="http://dx.doi.org/10.3389/fneur.2017.00455"
}