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Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice
Author(s) -
Kenne Ellinor,
Erlandsson Anna,
Lindbom Lennart,
Hillered Lars,
Clausen Fredrik
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.711.3
Subject(s) - extravasation , edema , evans blue , traumatic brain injury , medicine , pathology , microglia , infiltration (hvac) , cerebral edema , inflammation , blood–brain barrier , anesthesia , immunology , central nervous system , physics , psychiatry , thermodynamics
Brain edema as a result of secondary injury following traumatic brain injury (TBI) is a major clinical concern. Neutrophils are known to cause increased vascular permeability leading to edema formation in peripheral tissue, but their role in the pathology following TBI remains unclear. In this study we used controlled cortical impact (CCI) as a model for TBI and investigated the role of neutrophils in the response to injury. The outcome of mice that were depleted of neutrophils using anti‐Gr‐1 antibody was compared to that in mice with intact neutrophil count. Brain edema formation was assessed by Evan's blue dye extravasation and analysis of brain water content. Immunohistochemistry was used to assess cell death and microglial activation. Lesion volume was measured 7 and 14 days after CCI. Neutrophil‐depletion did not significantly affect Evan's blue extravasation at 24 or 48 hours after CCI. However, neutrophil‐depleted mice exhibited decreased water content both at 24 and 48 hours after CCI indicating reduced edema formation. Additionally, neutropenic mice had a decreased number of activated microglia, and brain tissue loss was attenuated in these mice. Furthermore, the number apoptotic cells 24 h after injury was significantly reduced in neutrophil depleted mice. Our results suggest that neutrophils play a role in the edema formation and contribute to the cell death and tissue loss following TBI.