Table 1 Summary of clinical studies investigating the role of complement in TBI
From: Correction to: the role of the complement system in traumatic brain injury: a review
Study | Type of brain insult | Controls | Assay | Complement pathway(s) | Relevant finding(s) |
|---|---|---|---|---|---|
Bellander et al., 2001 [23] | Cerebral contusion (n=16) | Epileptic patients undergoing hippocampectomy (n=3) | Immunohistochemistry (IHC) for C1q, C3b, C3d and MAC; in situ hybridization for C3 mRNA | All | Increased immunoreactivity for C1q, C3b, C3d and the MAC in the immediate vicinity of neurons in the penumbra area of the contusion in the patient group. In situ hybridization revealed C3 mRNA in the penumbra. |
Kossmann et al., 1997 [74] | Severe TBI (n=13): closed head injury (n=12); open head injury (n=1) | Patients undergoing diagnostic lumbar puncture (n=22) | Radioimmunoassay (RIA) or enzyme linked immunosorbent assay (ELISA) for C3 and fB | All | Elevated levels of C3 and fB in CSF of TBI patients compared to controls. |
Stahel et al., 2001 [24] | Severe TBI (closed head injury) (n=11) | Patients, without any known head trauma or inflammatory neurological disease, undergoing diagnostic spinal tap (n=12) | ELISA for sC5b-9 | All | Raised mean sC5b-9 levels in CSF of 10 out of 11 TBI patients compared to CSF obtained from controls. |
Longhi et al., 2014 [75] | Cerebral contusion (n=6) | Non-TBI patients who received surgery for brain tumors (n=2) | IHC for MBL | Lectin | MBL-positive staining was observed in brain tissue samples from cerebral contusion patients, but not in equivalent samples from controls. |