Genetic Ablation of Toll-Like Receptor 2 Reduces Secondary Brain Injury Caused by Cortical Contusion in Mice

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Abstract

Previous studies have shown that Toll-like receptor 2 (TLR2) was up-regulated after traumatic brain injury (TBI), but the potential contribution of TLR2 to TBI still remains unclear. The present study investigated the role of TLR2 in modulating TBI-induced secondary brain injury in mice. Wildtype TLR2(+/+) and TLR2(-/-)-deficient mice were subjected to a moderately severe weight-drop impact head injury. Brain samples were extracted at 24 hours after trauma. We measured TLR2 by western blot; motor function by Grip test; brain edema by wet/dry method; cortical apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method; and IL-1β, TNF-α and IL-6 by enzyme-linked immunosorbent assay (ELISA). We found the absence of TLR2 function in mice resulted in ameliorating brain injury as shown by the reduced severity of neurological deficit, apoptosis, and brain edema at 24 hours after TBI, which was associated with the decreased expression of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), compared with their wildtype counterparts after TBI. In combination, these results suggest that TLR2 might play an important aggravating role in the pathogenesis of TBI-induced secondary brain injury, possibly by regulating inflammatory cytokines in the cortex.

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