Effect of leukocyte-endothelial adhesion antagonism on neutrophil migration and neurologic outcome after cortical trauma

Kyle D. Weaver, Craig A. Branch, Luis Hernandez, Claramae H. Miller, Keith B. Quattrocchi

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Administration of anti-CD11B, a monoclonal antibody directed against the leukocyte adhesion molecule CD11B, results in decreased neutrophil infiltration into injured tissue after experimental ischemia. We determined the effect of anti-CD11B administration on neutrophil migration and neurologic functioning after experimental cortical trauma. Methods: Injuries were produced by a pneumatic impactor. Treatment animals received anti-CD11B after injury. Neurologic functioning was quantitated at 1, 12, and 24 hours after injury. Neutrophil migration was assessed with the myeloperoxidase assay. Results: Neutrophil influx was increased in injured cortex after trauma. Anti-CD11B significantly reduced neutrophil influx. There was no significant improvement in neurologic functioning after MAb administration. Conclusions: These results show there is marked neutrophil response to injury as produced with the pneumatic contusion model. This migration may be significantly attenuated by administration of a anti-CD11B.

Original languageEnglish (US)
Pages (from-to)1081-1090
Number of pages10
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume48
Issue number6
StatePublished - Jun 2000
Externally publishedYes

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Nervous System
Neutrophils
Leukocytes
Wounds and Injuries
Neutrophil Infiltration
Contusions
Cell Adhesion Molecules
Peroxidase
Ischemia
Monoclonal Antibodies

Keywords

  • Animal models
  • Brain injury
  • Cellular adhesion molecules
  • Inflammation

ASJC Scopus subject areas

  • Surgery

Cite this

Effect of leukocyte-endothelial adhesion antagonism on neutrophil migration and neurologic outcome after cortical trauma. / Weaver, Kyle D.; Branch, Craig A.; Hernandez, Luis; Miller, Claramae H.; Quattrocchi, Keith B.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 48, No. 6, 06.2000, p. 1081-1090.

Research output: Contribution to journalArticle

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AU - Quattrocchi, Keith B.

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AB - Background: Administration of anti-CD11B, a monoclonal antibody directed against the leukocyte adhesion molecule CD11B, results in decreased neutrophil infiltration into injured tissue after experimental ischemia. We determined the effect of anti-CD11B administration on neutrophil migration and neurologic functioning after experimental cortical trauma. Methods: Injuries were produced by a pneumatic impactor. Treatment animals received anti-CD11B after injury. Neurologic functioning was quantitated at 1, 12, and 24 hours after injury. Neutrophil migration was assessed with the myeloperoxidase assay. Results: Neutrophil influx was increased in injured cortex after trauma. Anti-CD11B significantly reduced neutrophil influx. There was no significant improvement in neurologic functioning after MAb administration. Conclusions: These results show there is marked neutrophil response to injury as produced with the pneumatic contusion model. This migration may be significantly attenuated by administration of a anti-CD11B.

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