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Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage.

dc.contributor.author Dawson, Hana Nenicka
dc.contributor.author James, Michael Lucas
dc.contributor.author Laskowitz, Daniel Todd
dc.contributor.author Lei, Beilei
dc.contributor.author Roulhac-Wilson, B
dc.contributor.author Wang, Haichen
dc.coverage.spatial England
dc.date.accessioned 2017-05-01T17:21:10Z
dc.date.available 2017-05-01T17:21:10Z
dc.date.issued 2013-08-20
dc.identifier https://www.ncbi.nlm.nih.gov/pubmed/23962089
dc.identifier 1742-2094-10-103
dc.identifier.uri http://hdl.handle.net/10161/14240
dc.description.abstract BACKGROUND: Intracerebral hemorrhage (ICH) is a devastating stroke subtype characterized by a prominent neuroinflammatory response. Antagonism of pro-inflammatory cytokines by specific antibodies represents a compelling therapeutic strategy to improve neurological outcome in patients after ICH. To test this hypothesis, the tumor necrosis factor alpha (TNF-α) antibody CNTO5048 was administered to mice after ICH induction, and histological and functional endpoints were assessed. METHODS: Using 10 to 12-week-old C57BL/6J male mice, ICH was induced by collagenase injection into the left basal ganglia. Brain TNF-α concentration, microglia activation/macrophage recruitment, hematoma volume, cerebral edema, and rotorod latency were assessed in mice treated with the TNF-α antibody, CNTO5048, or vehicle. RESULTS: After ICH induction, mice treated with CNTO5048 demonstrated reduction in microglial activation/macrophage recruitment compared to vehicle-treated animals, as assessed by unbiased stereology (P = 0.049). This reduction in F4/80-positive cells was associated with a reduction in cleaved caspase-3 (P = 0.046) and cerebral edema (P = 0.026) despite similar hematoma volumes, when compared to mice treated with vehicle control. Treatment with CNTO5048 after ICH induction was associated with a reduction in functional deficit when compared to mice treated with vehicle control, as assessed by rotorod latencies (P = 0.024). CONCLUSIONS: Post-injury treatment with the TNF-α antibody CNTO5048 results in less neuroinflammation and improved functional outcomes in a murine model of ICH.
dc.language eng
dc.relation.ispartof J Neuroinflammation
dc.relation.isversionof 10.1186/1742-2094-10-103
dc.subject Animals
dc.subject Antibodies, Monoclonal
dc.subject Cerebral Hemorrhage
dc.subject Disease Models, Animal
dc.subject Inflammation
dc.subject Male
dc.subject Mice
dc.subject Mice, Inbred C57BL
dc.subject Nervous System Diseases
dc.subject Random Allocation
dc.subject Recovery of Function
dc.subject Tumor Necrosis Factor-alpha
dc.title Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage.
dc.type Journal article
pubs.author-url https://www.ncbi.nlm.nih.gov/pubmed/23962089
pubs.begin-page 103
pubs.organisational-group Anesthesiology
pubs.organisational-group Anesthesiology, Neuroanesthesia
pubs.organisational-group Basic Science Departments
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Clinical Research Institute
pubs.organisational-group Institutes and Centers
pubs.organisational-group Neurobiology
pubs.organisational-group Neurology
pubs.organisational-group Neurology, Neurocritical Care
pubs.organisational-group Neurosurgery
pubs.organisational-group School of Medicine
pubs.publication-status Published online
pubs.volume 10
dc.identifier.eissn 1742-2094


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