Expression of endothelial adhesion molecules and recruitment of neutrophils after traumatic brain injury in rats.

摘要: Traumatic brain injury (FBI) is often ac- companied by an acute inflammatory reaction medi- ated initially neutrophils. Adhesion molecules ex- pressed on vascular endothelium are requisite elements during recruitment of leukocytes at sites inflam- mation. In a rat model TBI the induction and per- sistent expression E-selectin (CD62E) cerebro- ipsilateral, but not contralateral, to site contusion was demonstrated (P < 0.05 4 48 h posttrauma). addition, these studies confirmed up-regulation prolonged ICAM-1 (CD54) in traumatized hemisphere 4, 24, 48, 72 post- trauma). It interest that increased CD54 noted blood vessels non-traumatized posurauma. Ex- pression third endothelial adhesion molecule, PECAM-1 (CD31), unchanged following trauma. Administration murine monoclonal antibody (TM-8) inhibits adhesive function blocked significant portion (37.9%) neutrophil 24 posttrauma = 0.04). Employing immunocytochemistry spe- cffic for neutrophils (RP-3), peak infiltration shown occur after contrast emigration from yes- sels within contusion, howeyer, entry neutro- plith occurred surrounding leptomeninges choroidal yessels. These demonstrate relevance ofCD54 (ICAM-!) phiL; TBI. However, majority influx relies other than CD54. Because predominantly choroid plexus, intrathecal deliy- ery agents inhibit adhesiye interactions be- tween neutrophils, CD54, endo- thelial be defined may offer novel form oftherapy prevent response follows J. Leukoc. Biol. 61: 279- 285; 1997.