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

Publication ,  Journal Article
Lei, B; Dawson, HN; Roulhac-Wilson, B; Wang, H; Laskowitz, DT; James, ML
Published in: J Neuroinflammation
August 20, 2013

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.

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Published In

J Neuroinflammation

DOI

EISSN

1742-2094

Publication Date

August 20, 2013

Volume

10

Start / End Page

103

Location

England

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Recovery of Function
  • Random Allocation
  • Neurology & Neurosurgery
  • Nervous System Diseases
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Inflammation
  • Disease Models, Animal
 

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Lei, B., Dawson, H. N., Roulhac-Wilson, B., Wang, H., Laskowitz, D. T., & James, M. L. (2013). Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage. J Neuroinflammation, 10, 103. https://doi.org/10.1186/1742-2094-10-103
Lei, Beilei, Hana N. Dawson, Briana Roulhac-Wilson, Haichen Wang, Daniel T. Laskowitz, and Michael L. James. “Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage.J Neuroinflammation 10 (August 20, 2013): 103. https://doi.org/10.1186/1742-2094-10-103.
Lei B, Dawson HN, Roulhac-Wilson B, Wang H, Laskowitz DT, James ML. Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage. J Neuroinflammation. 2013 Aug 20;10:103.
Lei, Beilei, et al. “Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage.J Neuroinflammation, vol. 10, Aug. 2013, p. 103. Pubmed, doi:10.1186/1742-2094-10-103.
Lei B, Dawson HN, Roulhac-Wilson B, Wang H, Laskowitz DT, James ML. Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage. J Neuroinflammation. 2013 Aug 20;10:103.
Journal cover image

Published In

J Neuroinflammation

DOI

EISSN

1742-2094

Publication Date

August 20, 2013

Volume

10

Start / End Page

103

Location

England

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Recovery of Function
  • Random Allocation
  • Neurology & Neurosurgery
  • Nervous System Diseases
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Inflammation
  • Disease Models, Animal