Lechner F, Sahrbacher U, Suter T, Frei K, Brockhaus M, Koedel U, Fontana A
Cytos Biotechnology AG, CH-8952 Zurich-Schlieren, Switzerland.
J Infect Dis. 2000 Sep;182(3):978-82. doi: 10.1086/315765. Epub 2000 Aug 17.
A hallmark of infectious meningitis is the invasion of leukocytes into the subarachnoid space. In experimental meningitis triggered by tumor necrosis factor-alpha and interleukin-1beta, the interaction of leukocytes with endothelial cells and the subsequent migration of the cells through the vessel wall can be inhibited by an antibody to the junctional adhesion molecule (JAM). In contrast to the cytokine-induced meningitis model, anti-JAM antibodies failed to prevent leukocyte influx into the central nervous system after infection of mice with Listeria monocytogenes or lymphocytic choriomeningitis virus. Furthermore, in bacterial meningitis, anti-JAM IgG antibodies, but not Fab fragments, caused disruption of the endothelium. Likewise complement-dependent antibody-mediated cytotoxicity was observed in cultured brain endothelial cells treated with anti-JAM IgG but not with its Fab fragment.
感染性脑膜炎的一个标志是白细胞侵入蛛网膜下腔。在由肿瘤坏死因子-α和白细胞介素-1β引发的实验性脑膜炎中，白细胞与内皮细胞的相互作用以及随后细胞穿过血管壁的迁移可被一种针对连接黏附分子（JAM）的抗体所抑制。与细胞因子诱导的脑膜炎模型不同，在用单核细胞增生李斯特菌或淋巴细胞性脉络丛脑膜炎病毒感染小鼠后，抗JAM抗体未能阻止白细胞流入中枢神经系统。此外，在细菌性脑膜炎中，抗JAM IgG抗体而非Fab片段会导致内皮细胞破坏。同样，在用抗JAM IgG而非其Fab片段处理的培养脑内皮细胞中观察到了补体依赖性抗体介导的细胞毒性。
