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Updated: Aug 8, 2026
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
Published on: June 20, 2017
Effect of traumatic brain injury in mice deficient in intercellular adhesion molecule-1: assessment of
M J Whalen1, T M Carlos, C E Dixon
1Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh, Pennsylvania, USA.
Insights
Intercellular adhesion molecule-1 (ICAM-1) did not impact outcomes in traumatic brain injury (TBI) models. Studies found no differences in neutrophil accumulation or injury severity between ICAM-1 deficient and wild-type mice after TBI.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Intercellular adhesion molecule-1 (ICAM-1) is upregulated in the brain during acute inflammatory responses to traumatic brain injury (TBI).
- ICAM-1 is known to mediate neurological damage in experimental meningitis and stroke models.
Purpose of the Study:
- To investigate the role of ICAM-1 in the pathogenesis of TBI.
- To determine if ICAM-1 deficiency impacts neutrophil accumulation, histological injury, and neurological outcomes following TBI.
Main Methods:
- Controlled cortical impact (CCI) was used to induce TBI in ICAM-1 deficient (-/-) and wild-type (+/+) mice.
- Neutrophil accumulation and ICAM-1 expression were assessed via immunohistochemistry.
- Motor and cognitive functions were evaluated using the wire grip test and Morris water maze (MWM).
- Lesion volume was quantified 21 days post-TBI.
Main Results:
- ICAM-1 expression was confirmed in wild-type mice but absent in deficient mice post-TBI.
- No significant differences were observed in brain neutrophil accumulation between the groups.
- Motor and cognitive functional tests showed no significant differences between ICAM-1 deficient and wild-type mice.
- Lesion volumes were comparable in both groups 21 days after TBI.
Conclusions:
- The study failed to demonstrate a significant role for ICAM-1 in the pathogenesis of TBI.
- ICAM-1 deficiency did not alter neutrophil infiltration, histological damage, or functional recovery after experimental TBI.
Abstract:
Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule of the immunoglobulin family expressed on endothelial cells that is upregulated in brain as part of the acute inflammatory response to traumatic brain injury (TBI). ICAM-1 mediates neurologic injury in experimental meningitis and stroke; however, its role in the pathogenesis of TBI is unknown. We hypothesized that mutant mice deficient in ICAM-1 (-/-) would have decreased neutrophil accumulation, diminished histologic injury, and improved functional neurologic outcome versus ICAM-1 +/+ wild type control mice after TBI. Anesthetized ICAM-1 -/- mice and wild-type controls were subjected to controlled cortical impact (CCI, 6 m/sec, 1.2 mm depth). Neutrophils in brain parenchyma and ICAM-1 on vascular endothelium were assessed by immunohistochemistry in cryostat brain sections from the center of the contusion 24 h after TBI (n = 4/group). Separate groups of wild-type and ICAM-1-deficient mice (n = 9-10/group) underwent motor (wire grip test, days 1-5) and cognitive (Morris water maze [MWM], days 14-20) testing. Lesion volume was determined by image analysis 21 days following TBI. Robust expression of ICAM-1 was readily detected in choroid plexus and cerebral endothelium at 24 h in ICAM-1 +/+ mice but not in ICAM-1 -/- mice. No differences between groups were observed in brain neutrophil accumulation (9.4 +/- 2.2 versus 11.1 +/- 3.0 per x100 field, -/- versus +/+), wire grip score, MWM latency, or lesion volume (7.24 +/- 0.63 versus 7.21 +/- 0.45 mm3, -/- versus +/+). These studies fail to support a role for ICAM-1 in the pathogenesis of TBI.
