gms | German Medical Science

60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

Role of toll-like receptors for the secondary growth of a necrosis following experimental traumatic brain injury

Meeting Abstract

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  • F. Voigt - Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar der TU München
  • N. Plesnila - Department of Neurodegeneration, Royal College of Surgeons in Ireland, Dublin
  • B. Meyer - Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar der TU München
  • F. Ringel - Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar der TU München

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMO.13-03

DOI: 10.3205/09dgnc091, URN: urn:nbn:de:0183-09dgnc0918

Published: May 20, 2009

© 2009 Voigt et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

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Objective: Toll-like receptors (TLR) are key receptors of the innate immune response to external pathogens. In addition, TLR respond to intrinsic ligands leading to an immune response in the sequelae of an ischemic damage. This was also shown for ischemic brain injury where TLR activation was associated with the increase of tissue damage. Thus, a possible activation of TLR after traumatic brain injury might contribute to the secondary expansion of a traumatic brain lesion.

Methods: C57Bl6 wildtype mice, TLR 2/4 double-knockout mice as well as TLR 9 knockout mice were exposed to a controlled coritical impact injury of the brain. Fifteen minutes and 24h after trauma, the size of the resulting brain tissue necrosis was measured or the extent of the traumatic brain edema determined by water content measurement.

Results: Mice lacking Toll-like-receptors 2 and 4 developed a 20.5 percent smaller lesion within 24h after controlled cortical impact injury (p<0.0052). However, there was no difference in the extent of traumatic brain edema between TLR 2/4 k.o. and wild-type mice. Also TLR 9 deficiency leads to a reduction of lesion size of 12.3 percent ( p<0.0054 ) within 24h after trauma. Preconditiong wild-type mice by injecting CpG nucleotides (stimulating or antagonizing TLR 9 24 hours before controlled cortical impact injury showed no significant effects on lesion size.

Conclusions: Our data indicate that TLR 2, 4 and 9 signalling is associated with the delayed expansion of a cortical contusion following traumatic brain injury. A further analysis of the underlying immunological processes is currently in progress.