ADHESION MOLECULE EXPRESSION ON MURINE CEREBRAL ENDOTHELIUM FOLLOWING THE INJECTION OF A PROINFLAMMAGEN OR DURING ACUTE NEURONAL DEGENERATION
ADHESION MOLECULE EXPRESSION ON MURINE CEREBRAL ENDOTHELIUM FOLLOWING THE INJECTION OF A PROINFLAMMAGEN OR DURING ACUTE NEURONAL DEGENERATION
复制标题
DOI：
10.1007/bf01179819
复制
发表时间：
1995-09-01
期刊：
影响因子：
--
通讯作者：
PERRY, VH
中科院分区：
文献类型：
--
作者：
BELL, MD;PERRY, VH
小鼠CNS中的急性炎症反应与在其他组织中观察到的不同。很少有多形核白细胞被募集到脑实质，单核细胞的募集也有延迟。白细胞向炎症部位的募集依赖于内皮上表达的粘附分子。白细胞向CNS募集的非典型动力学可能是脑内皮细胞上粘附分子表达不足或延迟的结果。使用免疫组织化学，本研究表明，颅内注射后的促炎原，脂多糖，或以下急性神经元变性引起的红藻氨酸，粘附分子ICAM-1和VCAM很容易上调脑内皮细胞在一个时间过程中表现出与非CNS内皮细胞。在红藻氨酸注射后24小时或脂多糖注射后6小时，两种分子均在血管上表达，无论其大小，但白细胞募集可忽略不计。ICAM-1不仅在内皮细胞上表达，而且在小胶质细胞上也有表达，特别是在神经末梢变性时。PECAM在脑内皮细胞上组成性高水平表达，在脑损伤过程中没有变化。然而，PECAM诱导星形胶质细胞脂多糖注射后或在急性神经元变性，后者提供了一个特别强的刺激。这项研究表明，这些粘附分子在中枢神经系统内皮细胞上的表达既不缺乏也不延迟，它们不太可能是白细胞向中枢神经系统募集的限制因素。
The acute inflammatory response in the murine CNS is different from that observed in other tissues. Few polymorphonuclear leukocytes are recruited to the brain parenchyma and there is a delay in the recruitment of monocytes. Leukocyte recruitment to sites of inflammation is dependent on adhesion molecules expressed on the endothelium. The atypical kinetics of leukocyte recruitment to the CNS may be the result of deficient or delayed adhesion molecule expression on the cerebral endothelium. Using immunohistochemistry, the present study demonstrates that following the intracranial injection of a proinflammagen, Lipopolysaccharide, or following acute neuronal degeneration elicited with kainic acid, the adhesion molecules ICAM-1 and VCAM were readily upregulated on cerebral endothelium in a time course comparable with that demonstrated on non-CNS endothelium. Both molecules were expressed on vessels, irrespective of their size, at 24h after kainic acid or 6h after Lipopolysaccharide injection but leukocyte recruitment was negligible. The expression of ICAM-1 was demonstrated not only on endothelium but also on microglia especially in response to nerve terminal degeneration. PECAM was constitutively expressed at high levels on cerebral endothelium and did not change during brain injury. However, PECAM was induced on astrocytes after lipopolysaccharide injection or during acute neuronal degeneration, the latter providing a particularly strong stimulus. This study indicates that the expression of these adhesion molecules on CNS endothelium is neither deficient or delayed and that they are unlikely to be limiting factors in leukocyte recruitment to the CNS.