SOLUBLE ICAM-1 IN CSF COINCIDES WITH THE EXTENT OF CEREBRAL-DAMAGE INPATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY

The intercellular adhesion molecule-1 (ICAM-1) expressed by endothelia l cells is crucial in promoting adhesion and transmigration of circula ting leukocytes across the blood-brain barrier (BBB), Migrated immunoc ompetent cells, in turn, release mediators that stimulate glial and en dothelial cells to express ICAM-1 and release cytokines, possibly sust aining cerebral damage. Following activation, proteolytic cleavage of membrane-anchored ICAM-1 results in measurable levels of a soluble for m, sICAM-1, The aims of this study were to investigate the changes of sICAM-1 levels in ventricular CSF and serum and to elucidate the influ ence of structural brain damage as estimated by computerized tomograph y (CT) as well as the extent of BBB dysfunction as calculated by the C SF/serum albumin ratio (Q(A)) in patients with severe traumatic brain injury (TBI), All investigated parameters revealed two subgroups, Pati ents belonging to group A had sICAM-1 levels in CSF above normal range , presented marked cerebral damage and a disturbance of the BBB (range 0.6-24.7 ng/ml, n = 8), In contrast, patients belonging to group B ha d no elevation of sICAM-1 values in CSF (range 0.3-3.9 ng/ml, n = 5; p < 0.017) acid showed minor cerebral damage with an intact BBB in most cases. In addition, overall analysis showed that sICAM-1 in CSF corre lated with the extent of BBB damage as indicated by the Q(A) (r = 10.7 6; P < 0.001), These results suggest that increased sICAM-1 levels in CSF might depict ongoing immunologic activation and that sICAM-1 corre lates with the extent of tissue and BBB damage. The origin of soluble ICAM-1 in CSF and its pathophysiologic role after TBI remains to be cl arified.