Spinal cord injury in ICAM-1-deficient mice: assessment of functional and histopathological outcome

Adhesion molecule-mediated adhesion and extravasation of leukocytes may constitute a mechanism of secondary tissue damage following spinal cord injury (SCI). The objective of the present study was to determine to what extent genetic deficiency in the adhesion molecule ICAM-1 influences functional and histopathological measures of outcome following SCI. ICAM-1-/- (n = 11) and wild-type (n = 9) mice were subjected to a compression-type SCI. Assessment of hind-limb motor function was done on days 1, 2, 4, 7, 10, and 14 after injury, using a motor function scoring system. Injury resulted in a drastically impaired hind limb motor function at day one after injury followed by a partial recovery during the observation period. No significant functional differences were found between the experimental groups at any time-point. Fourteen days after injury the animals were sacrificed and the spinal cords were processed for histopathological and immunohistochemical evaluation. Luxol-stained, MAP2-, GFAP- and iba-1-immunostained cross-sectional areas were quantitated using a computerized image analysis system to investigate white matter damage, neuronal loss, astrocytic response and microglial activation respectively. None of these parameters differed significantly between the groups. Separate experiments revealed that the early (24 h postinjury) infiltration of polymorphonuclear leukocytes was significantly reduced in white matter but not in the grey matter of ICAM-1-/- mice, compared to injured controls. In summary, these results do not support the concept that ICAM-1 alone mediates secondary tissue damage following traumatic SCI in the mouse.