• Deborah Bingham, Constance M John, Jack Levin, S Scott Panter, and Gary A Jarvis.
• Center for Immunochemistry, 4150 Clement Street, Veterans Affairs Medical Center, San Francisco, CA 94121, USA.
• J. Neuroimmunol. 2013 Mar 15; 256 (1-2): 28-37.

BackgroundTraumatic brain injury (TBI) is a leading cause of mortality and disability in the Western world. The first stage of TBI results from the mechanical damage from an impact or blast. A second stage occurs as an inflammatory response to the primary injury and presents an opportunity for clinical intervention. In this study, we investigated the effect of pre- and post-injury treatment with lipopolysaccharide (LPS) from Escherichia coli and lipooligosaccharide (LOS) from Neisseria meningitidis on levels of cerebral inflammatory cells, circulating blood cells, and pro- and anti-inflammatory cytokine levels in a rat model of neuroinflammation induced by intrastriatal injection of IL-1β to mimic the second stage of TBI.MethodsLPS or LOS was administered intravenously (IV) or intranasally (IN) 2h pre- or post-injection of IL-1β. The rats were euthanized 12h following IL-1β injection. Brain sections were immunostained with antibody to ED-1, a microglia cell marker. Cells in whole blood were assessed with a VetScan HM2 analyzer, and cytokine levels in sera were analyzed with a Bio-Plex system.ResultsPre- and post-injury IV administration of LPS or LOS significantly reduced microglia in the brain, and IN pre-treatment with LPS or LOS showed a statistical trend towards reducing microglia. Pre- and post-treatment IV with LOS increased circulating levels of IL-2 and IL-4, whereas IN post-treatment with LPS reduced levels of the inflammatory cytokines, TNF-α and IFN-γ.ConclusionsThe findings strongly support continued investigation of post-conditioning with LPS or LOS as potential neuroprotective treatments for neuroinflammation from TBI.Published by Elsevier B.V.

33 keywords...

hide…