• Elham Rostami, Johan Davidsson, Andrea Gyorgy, Denes V Agoston, Mårten Risling, and Bo-Michael Bellander.
• 1 Department of Neuroscience, Karolinska Institutet , Stockholm, Sweden .
• J. Neurotrauma. 2013 Dec 1;30(23):1954-65.

AbstractThe complement system plays an important role in the inflammatory response activated by many central nervous system disorders. However, its significance in traumatic diffuse traumatic axonal injury (TAI) is not fully known. Here we analyze the complement activity in two rat models of traumatic brain injury (TBI); a focal penetration injury (pen-TBI) and a rotational acceleration injury (rot-TBI) that leads to a mild TAI. We used in situ hybridization to examine the distribution of mRNA for C1q and C3 and immunohistochemistry to examine the presence of the C3 protein and C5b-9 complex at 1-5 days after injury. We found a time-dependent complement activity in both models. However, the responses caused by the two models were different. We detected C5b-9 surrounding the cavity in pen-TBI, but C5b-9 was not found in the rot-TBI. Our findings suggest that the terminal complement pathway is progressed to the formation of the C5b-9 membrane attack complex only in the penetrating TBI but not in isolated TAI model. This indicates that the complement activation does not lead to membrane-damaging effects and a subsequent secondary axotomy in TAI by the terminal complex C5b-9. The role of complement activation in TAI is unclear, but might indicate an alternative function following rot-TBI, such as opsonizing the synapses for elimination.

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