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- Title:
Decreased Secondary Lesion Growth and Attenuated Immune Response after Traumatic Brain Injury in Mice.
- Document type:
- Journal Article
- Author(s):
- Krieg, Sandro M; Voigt, Florian; Knuefermann, Pascal; Kirschning, Carsten Jürgen; Plesnila, Nikolaus; Ringel, Florian
- 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 and wild-type (WT) mice. 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 mice (29.7 ± 0.7 mm as compared to 33.5 ± 0.8 mm in WT; < 0.05) after CCI while brain edema was not affected. Only interleukin (IL)-1? gene expression was increased after CCI in the relative to WT mice. Inducible nitric oxide synthetase, TNF, IL-6, and COX-2 were similar in injured WT and 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 neuroinflammation and may therefore represent a novel therapeutic target for the treatment of TBI.
- Journal title abbreviation:
- Front Neurol
- Year:
- 2017
- Journal volume:
- 8
- Pages contribution:
- 455
- Language:
- eng
- Fulltext / DOI:
- doi:10.3389/fneur.2017.00455
- Pubmed ID:
- http://view.ncbi.nlm.nih.gov/pubmed/28912751
- Print-ISSN:
- 1664-2295
- TUM Institution:
- Neurochirurgische Klinik und Poliklinik
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