PMID- 24858498 OWN - NLM STAT- MEDLINE DCOM- 20151015 LR - 20220129 IS - 1559-1174 (Electronic) IS - 1535-1084 (Linking) VI - 16 IP - 3 DP - 2014 Sep TI - Endothelial activation and chemoattractant expression are early processes in isolated blast brain injury. PG - 606-19 LID - 10.1007/s12017-014-8313-y [doi] AB - Blast injuries are an increasing problem in military conflicts and terrorist incidents. Blast-induced traumatic brain injury has risen to prominence and represents a specific form of primary brain injury, with sufficiently different physical attributes (and possibly biological consequences) to be classified separately. There is increasing interest in the role of blast in initiating inflammatory responses, which may be linked to the pathological processes seen clinically. Terminally anaesthetised rats were exposed to a blast wave directed at the cranium, using a bench-top blast wave generator. Control animals were not exposed to blast. Animals were killed after 8 h, and the brains examined for evidence of an inflammatory response. Compared to controls, erythropoietin, endothelial integrins, ICAM and sVCAM, and the pro-inflammatory cytokine, monocyte chemoattractant protein-1 (MCP-1) were significantly elevated. Other pro-inflammatory cytokines, including MIP-1alpha, were also detectable, but levels did not permit accurate quantification. Six inflammatory genes examined by qRT-PCR exhibited a biologically significant increase in activity in the blast-exposed animals. These included genes supporting chemokines responsible for monocyte recruitment, including MCP-1, and chemokines influencing T cell movement. Brain injury is usually accompanied by pathological neuro-inflammation. This study shows that blast brain injury is no exception, and the data provide important mechanistic clues regarding the drivers of such inflammation. Whilst this effect alone is unlikely to be responsible for the totality of consequences of blast brain injury, it suggests a mechanism that may be priming the cerebral inflammatory response and rendering cerebral tissue more susceptible to the deleterious effects of systemic inflammatory reactions. FAU - Risdall, Jane E AU - Risdall JE AD - University Department of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Hills Road, Box 93, Cambridge, CB2 0QQ, UK, jer56@cam.ac.uk. FAU - Carter, Alun J AU - Carter AJ FAU - Kirkman, Emrys AU - Kirkman E FAU - Watts, Sarah A AU - Watts SA FAU - Taylor, Christopher AU - Taylor C FAU - Menon, David K AU - Menon DK LA - eng GR - G0001354/MRC_/Medical Research Council/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20140525 PL - United States TA - Neuromolecular Med JT - Neuromolecular medicine JID - 101135365 RN - 0 (Ccl2 protein, rat) RN - 0 (Cell Adhesion Molecules) RN - 0 (Chemokine CCL2) RN - 0 (Cytokines) RN - 0 (Integrins) RN - 11096-26-7 (Erythropoietin) SB - IM MH - Animals MH - Blast Injuries/*metabolism/pathology MH - Brain Injuries/etiology/*metabolism/pathology MH - Cell Adhesion Molecules/*biosynthesis/genetics MH - Chemokine CCL2/biosynthesis/genetics MH - Chemotaxis, Leukocyte/genetics MH - Cytokines/*biosynthesis/genetics MH - Encephalitis/etiology/*metabolism MH - Endothelium, Vascular/pathology/*physiopathology MH - Erythropoietin/*biosynthesis/genetics MH - Gene Expression Regulation MH - Hemodynamics MH - Integrins/*biosynthesis/genetics MH - Male MH - Random Allocation MH - Rats MH - Rats, Wistar MH - T-Lymphocytes/physiology EDAT- 2014/05/27 06:00 MHDA- 2015/10/16 06:00 CRDT- 2014/05/27 06:00 PHST- 2014/02/03 00:00 [received] PHST- 2014/05/14 00:00 [accepted] PHST- 2014/05/27 06:00 [entrez] PHST- 2014/05/27 06:00 [pubmed] PHST- 2015/10/16 06:00 [medline] AID - 10.1007/s12017-014-8313-y [doi] PST - ppublish SO - Neuromolecular Med. 2014 Sep;16(3):606-19. doi: 10.1007/s12017-014-8313-y. Epub 2014 May 25.