title: Controlled cortical impact and craniotomy induce strikingly similar profiles of inflammatory gene expression, but with distinct kinetics.
abstract: An immediate consequence of traumatic brain injury (TBI) is the induction of an inflammatory response. Mounting data suggest that inflammation is a major contributor to TBI-induced brain damage. However, much remains unknown regarding the induction and regulation of the inflammatory response to TBI. In this study we compared the TBI-induced inflammatory response to severe parenchymal injury (controlled cortical impact) vs. mild brain injury (craniotomy) over a 21-day period. Our data show that both severe and mild brain injury induce a qualitatively similar inflammatory response, involving highly overlapping sets of effector molecules. However, kinetic analysis revealed that the inflammatory response to mild brain injury is of much shorter duration than the response to severe TBI. Specifically, the inflammatory response to severe brain injury persists for at least 21 days, whereas the response to mild brain injury returns to near baseline values within 10 days post-injury. Our data therefore imply that the development of accurate diagnostic tests of TBI severity that are based on imaging or biomarker analysis of the inflammatory response may require repeated measures over at least a 10-day period, post-injury.
authors.affiliation: Department of Microbiology and Immunology, Uniformed Services University Bethesda, MD, USA ; Center for Neuroscience and Regenerative Medicine, Uniformed Services University Bethesda, MD, USA.
authors.forename: Mouna
authors.initials: M
authors.lastname: Lagraoui
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Latoche
authors.forename: Natalia G
authors.initials: NG
authors.lastname: Cartwright
authors.forename: Gauthaman
authors.initials: G
authors.lastname: Sukumar
authors.forename: Clifton L
authors.initials: CL
authors.lastname: Dalgard
authors.forename: Brian C
authors.initials: BC
authors.lastname: Schaefer
keywords: cytokines; diagnostics; genomics; glia; inflammation; mouse models; response to injury; traumatic brain injury