Weber J R, Angstwurm K, Bürger W, Einhäupl K M, Dirnagl U
Department of Neurology, Universitätsklinikum Charité, Humboldt University Berlin, Germany.
J Neuroimmunol. 1995 Dec;63(1):63-8. doi: 10.1016/0165-5728(95)00131-x.
We investigated whether monoclonal antibodies directed against intracellular adhesion molecule 1 (ICAM-1 mAb) inhibit brain edema, increase of intracranial pressure (ICP), regional cerebral blood flow (rCBF) and recruitment of white blood cells (WBC) into the cerebrospinal fluid (CSF) in the rat model of the early phase of bacterial meningitis. Brain edema was assessed by brain water content determinations. rCBF measured by laser Doppler flowmetry and ICP were recorded continuously for 6 h after intracisternal challenge. Meningitis was induced with pneumococcal cell walls (PCW). Increase of ICP and brain water content were significantly inhibited (P <0.05) by intravenous treatment with ICAM-1 mAb (TM-8, 1 mg/kg). Furthermore, ICAM-1 mAb treatment profoundly attenuated (P <0.05) rCBF increase and WBC invasion into the CSF. These results suggest that the ICAM-1 pathway is critically involved in the early phase of bacterial meningitis.
我们研究了针对细胞间黏附分子1的单克隆抗体（ICAM-1单克隆抗体）是否能抑制细菌性脑膜炎早期大鼠模型中的脑水肿、颅内压（ICP）升高、局部脑血流量（rCBF）以及白细胞（WBC）向脑脊液（CSF）中的募集。通过测定脑含水量评估脑水肿。在脑池内注射后，用激光多普勒血流仪测量rCBF，并连续记录6小时的ICP。用肺炎球菌细胞壁（PCW）诱导脑膜炎。静脉注射ICAM-1单克隆抗体（TM-8，1mg/kg）可显著抑制ICP升高和脑含水量增加（P<0.05）。此外，ICAM-1单克隆抗体治疗可显著减轻（P<0.05）rCBF升高和WBC侵入CSF。这些结果表明，ICAM-1途径在细菌性脑膜炎的早期阶段起关键作用。
