Intracerebral cytokine production is thought to be partially responsible for the brain edema and increased leukocyte adhesion seen after head injury by both a direct effect on vascular permeability and by causing leukocyte activation. Cerebrospinal fluid concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 are elevated after traumatic brain injury. The cerebral endothelium has not been investigated as a de novo source of cytokines after injury. We have found that conditioned media from cultured human cerebral microvascular endothelium (HCME) subjected to percussion trauma increases neutrophil chemotaxis. To test the hypothesis that percussive trauma increases the production of TNF-α and IL-1β by HCME, serial supernatant samples from passage 2 HCME were collected for 24 hours and analyzed for TNF-α and IL-1β concentration by enzyme-linked immunosorbent assay after trauma. HCME subjected to percussion injury secreted significantly more TNF-α at 8 and 24 hours and significantly more IL-1β at 4 and 24 hours compared with uninjured controls (p < 0.05, Student's t test). These data suggest that HCME production of inflammatory cytokines occurs after traumatic brain injury independent of systemic influences. In situ cytokine production by HCME after percussion trauma may mediate the increased cerebral leukocyte accumulation and cerebrovascular dysfunction observed after focal brain injury.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Jun 1997|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine