Pro-inflammatory and pro-apoptotic elements of the neuroinflammatory response are activated in traumatic brain injury
JC Goodman, M Van, SP Gopinath… - Acta Neurochirurgica …, 2009 - Springer
JC Goodman, M Van, SP Gopinath, CS Robertson
Acta Neurochirurgica Supplements, 2009•SpringerBackground The inflammatory response may contribute to cerebral edema, increased
intracranial pressure and cellular loss in traumatic brain injury (TBI). Cytokines are
biomarkers of this inflammatory response and new methods allow simultaneous
measurement of multiple cytokines. Methods We examined the IL-1β, IL-6, IL-8 and IL-12,
TNFα, and IL-10 in arterial and jugular blood as well as cerebrospinal fluid in patients with
severe traumatic brain injury. Findings Multiple cytokines, particularly pro-inflammatory …
intracranial pressure and cellular loss in traumatic brain injury (TBI). Cytokines are
biomarkers of this inflammatory response and new methods allow simultaneous
measurement of multiple cytokines. Methods We examined the IL-1β, IL-6, IL-8 and IL-12,
TNFα, and IL-10 in arterial and jugular blood as well as cerebrospinal fluid in patients with
severe traumatic brain injury. Findings Multiple cytokines, particularly pro-inflammatory …
Background The inflammatory response may contribute to cerebral edema, increased intracranial pressure and cellular loss in traumatic brain injury (TBI). Cytokines are biomarkers of this inflammatory response and new methods allow simultaneous measurement of multiple cytokines.
Methods We examined the IL-1β, IL-6, IL-8 and IL-12, TNFα, and IL-10 in arterial and jugular blood as well as cerebrospinal fluid in patients with severe traumatic brain injury.
Findings Multiple cytokines, particularly pro-inflammatory cytokines, are up-regulated following TBI. Cerebrospinal fluid and arteriovenous differences of some of the cytokines suggest production within the central nervous system. Antiinflammatory cytokines are not up-regulated.
Conclusions Cytokine up-regulation may contribute to the neuroinflammatory reaction that follows traumatic brain injury and may contribute to secondary injury.
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