Matsuda M, Tsukada N, Miyagi K, Yanagisawa N
Department of Medicine (Neurology), Shinshu University School of Medicine, Matsumoto, Japan.
Int Arch Allergy Immunol. 1995 Apr;106(4):335-44. doi: 10.1159/000236863.
We investigated the in vitro adhesion of 51Cr-labeled lymphocytes to cultured brain endothelial cells and the in vivo expression of intercellular adhesion molecule-1 (ICAM-1) on cerebral endothelial cells in a rat model of experimental allergic encephalomyelitis (EAE) before and after treatment with lipopolysaccharide (LPS). Adhesion of lymphocytes to cerebral endothelial cells was significantly increased in EAE compared with controls (p < 0.01), and was significantly correlated with the percentage of major histocompatibility complex class II antigen-positive cells in lymph node cells (p < 0.001). LPS enhanced ICAM-1 expression on endothelial cells and lymphocyte adhesion to those cells, and caused a significant increase in the in vivo expression of ICAM-1 compared with controls (p < 0.001). Lymphocyte adhesion to endothelial cells was significantly blocked by monoclonal antibodies against ICAM-1, lymphocyte function-associated antigen-1, or very late activation antigen-4. Our findings suggest that lymphocyte adhesion to brain endothelial cells may contribute to lymphocyte migration across the blood-brain barrier in EAE and that LPS may cause progression of EAE lesions.
我们研究了在实验性变应性脑脊髓炎（EAE）大鼠模型中，用脂多糖（LPS）治疗前后，51Cr标记的淋巴细胞与培养的脑内皮细胞的体外黏附以及脑内皮细胞上细胞间黏附分子-1（ICAM-1）的体内表达。与对照组相比，EAE中淋巴细胞与脑内皮细胞的黏附显著增加（p < 0.01），且与淋巴结细胞中主要组织相容性复合体II类抗原阳性细胞的百分比显著相关（p < 0.001）。LPS增强了内皮细胞上ICAM-1的表达以及淋巴细胞与这些细胞的黏附，并导致ICAM-1的体内表达与对照组相比显著增加（p < 0.001）。抗ICAM-1、淋巴细胞功能相关抗原-1或极晚期活化抗原-4的单克隆抗体可显著阻断淋巴细胞与内皮细胞的黏附。我们的研究结果表明，淋巴细胞与脑内皮细胞的黏附可能有助于EAE中淋巴细胞穿越血脑屏障的迁移，并且LPS可能导致EAE病变进展。
