当前位置： SCI文献检索 > JOURNAL OF LEUKOCYTE BIOLOGY期刊下所有文献 > Expression of endothelial adhesion molecules and recruitment of neutrophils after traumatic brain injury in rats.

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

Abstract：

:Traumatic brain injury (TBI) is often accompanied by an acute inflammatory reaction mediated initially by neutrophils. Adhesion molecules expressed on vascular endothelium are requisite elements during recruitment of leukocytes at sites of inflammation. In a rat model of TBI the induction and persistent expression of E-selectin (CD62E) on cerebrovascular endothelium ipsilateral, but not contralateral, to the site of contusion was demonstrated (P < 0.05 at 4 and 48 h posttrauma). In addition, these studies confirmed up-regulation and prolonged expression of ICAM-1 (CD54) on endothelium in the traumatized hemisphere (P < 0.05 at 4, 24, 48, and 72 h posttrauma). It is of interest that increased expression of CD54 was noted on blood vessels in the contralateral, non-traumatized hemisphere 48 h posttrauma. Expression of a third endothelial adhesion molecule, PECAM-1 (CD31), was unchanged following trauma. Administration of a murine monoclonal antibody (TM-8) that inhibits the adhesive function of CD54 blocked a significant portion (37.9%) of neutrophil recruitment 24 h posttrauma (P = 0.04). Employing immunocytochemistry and a monoclonal antibody specific for rat neutrophils (RP-3), peak infiltration of neutrophils was shown to occur 48 h after trauma. In contrast to emigration of neutrophils from blood vessels within the contusion, however, entry of neutrophils occurred from the surrounding leptomeninges and choroidal vessels. These studies demonstrate the relevance of CD54 (ICAM-1) in recruitment of neutrophils following TBI. However, the majority of neutrophil influx relies on endothelial adhesion molecules other than CD54. Because emigration of neutrophils was shown to occur predominantly from vessels within the leptomeninges and choroid plexus, intrathecal delivery of agents that inhibit the adhesive interactions between neutrophils, endothelial CD54, and other endothelial adhesion molecules to be defined may offer a novel form of therapy to prevent the acute inflammatory response that follows TBI.

journal_name

J Leukoc Biol

journal_title

Journal of leukocyte biology

authors

Carlos TM,Clark RS,Franicola-Higgins D,Schiding JK,Kochanek PM

doi

10.1002/jlb.61.3.279

subject

Has Abstract

pub_date

1997-03-01 00:00:00

pages

279-85

issue

eissn

0741-5400

issn

1938-3673

journal_volume

pub_type

杂志文章

在线工具

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