| First Author | Krieg SM | Year | 2017 |
| Journal | Front Neurol | Volume | 8 |
| Pages | 455 | PubMed ID | 28912751 |
| Mgi Jnum | J:276735 | Mgi Id | MGI:6316430 |
| Doi | 10.3389/fneur.2017.00455 | Citation | Krieg SM, et al. (2017) Decreased Secondary Lesion Growth and Attenuated Immune Response after Traumatic Brain Injury in Tlr2/4(-/-) Mice. Front Neurol 8:455 |
| abstractText | 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)-1beta 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. |
