Increases in bcl-2 protein in cerebrospinal fluid and evidence for programmed cell death in infants and children after severe traumatic brain injury

Objectives: To determine whether bcl-2, a protein that inhibits apoptosis, would be increased in cerebrospinal fluid (CSF) in infants and children aft er traumatic brain injury (TBI) and to examine the association of bcl-2 con centration with clinical variables. Study design: Bcl-2 was measured in CSF from 23 children (aged 2 months-16 years) with severe TBI and from 19 children without TBI or meningitis (cont rol subjects) by enzyme-linked immunosorbent assay CSF oligonucleosome conc entration was also determined as a marker of DNA degradation. Brain samples from 2 patients undergoing emergent decompressive craniectomies were analy zed for bcl-2 with Western blot and for DNA fragmentation with TUNEL (termi nal deoxynucleotidyl-transerase mediated biotin-dUTP nick-end labeling). Results: CSF bcl-2 concentrations were increased in patients with TBI versu s control subjects (P = .01). Bcl-2 was increased in patients with TBI who survived versus those who died (P = .02). CSF oligonucleosome concentration tended to be increased after TBI (P = .07) and was not associated with bcl -2. Brain tissue samples showed an increase in bcl-2 in patients with TBI v ersus adult brain bank control samples and evidence of DNA fragmentation wi thin cells with apoptotic morphology Conclusions: Bcl-2 may participate in the regulation of cell, death after T BI in infants and children. The increase in bcl-2 seen in patients who surv ived is consistent with a protective role for this anti-apoptotic protein a fter TBI.