Activation of Complement Pathways after Contusion-Induced Spinal Cord Injury

• DOI: 10.1089/neu.2004.21.1831
• Publication Date: 2004-12-01T13:42:16Z
• Authors: Aileen J. Anderson; Stephanie Robert; Wencheng Huang; Wise Young; Carl W. Cotman
• Keywords: Complement factor B; Complement C1q

Previous studies have shown that a cellular inflammatory response is initiated, and cytokines are synthesized, following experimental spinal cord injury (SCI). In the present study, we tested hypothesis complement cascade, major component of both innate adaptive immune response, also activated SCI. We investigated pathways, localization, timecourse, degree activation in rat acute contusion-induced SCI using New York University (NYU) weight drop impactor. Mild severe injuries (12.5 50 mm heights) at 1, 7, 42 days post time points were evaluated. Classical (C1q C4), alternative (Factor B) terminal (C5b-9) pathways strongly within 1 day Complement protein immunoreactivity was predominantly found cell types vulnerable to degeneration, neurons oligodendrocytes, not generally observed or astroglial cells. Surprisingly, for proteins evident 6 weeks after injury, as far 20 rostral site injury. Axonal staining by C1q Factor B observed, suggesting potential role cascade demyelination axonal degeneration. These data support plays