Expression of ICAM-1 and CD11b after experimental spinal cord injury in rats

We have performed an immunohistochemical study on the expression of the adh esion molecules ICAM-1 and CD11b 1 h to 1 week following a compression inju ry to the rat spinal cord, The spinal cord of control animals showed ICAM-1 expression in some vessels and in the leptomeninges. Mechanical compressio n of the spinal cord induced an endothelial upregulation of ICAM-1 that was maximal in rats surviving 1-2 days after injury, This reaction was seen at the center of the lesion as well as in the perifocal zones, Apart from the endothelial upregulation, increased ICAM-1 expression also was found in le ptomeningeal and ependymal cells of traumatized animals. In control animals resting microglial cells were moderately CD11b immunoreactive. Trauma indu ced a rapid microglial upregulation of CD11b in the white matter that was e vident even at 1 h after injury, By 1 day to 1 week posttrauma conformation al changes consistent with microglial activation, i.e., transformation into phagocytic microglial cells, were seen in the white matter. In the gray ma tter, CD11b immunohistochemistry revealed massive infiltration of phagocyti c microglial cells and macrophages in animals surviving 1 day to 1 week, In travascular and infiltrating leukocytes were intensely CD11b immunopositive . As reflected by CD11b immunohistochemistry, the maximal infiltration of p olymorphonuclear leukocytes occurred at 2 days after the insult. Endothelia l upregulation of ICAM-1 facilitates adhesion and extravasation of leukocyt es by binding to the counterreceptor CD11b, Knowledge regarding the express ion and cellular distribution of such molecules after central nervous syste m trauma is important since inflammatory mechanisms have been suggested to be involved in secondary neurological damage and thus constitute potential targets of therapy.