ACUTE EXACERBATIONS OF MULTIPLE SCLEROSIS

多发性硬化症急性加重

• 批准号: 6264574
• 负责人: SUBRAMANIAM SRIRAM
• 金额: $ 0.06万
• 依托单位: VANDERBILT UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-12-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6264574
• 关键词: antiinflammatory agents; blood brain barrier; cell adhesion; clinical research; clinical trial phase I; human subject; human therapy evaluation; lymphocyte; multiple sclerosis; nervous system disorder chemotherapy; vascular endothelium

Multiple sclerosis is a chronic disease characterized by recurrent attacks of neurologyc dysfunction, due to lesions in the whate matter of the center nervous system. MS lesions evolve over time. "Active" lesions contain inflammatory cells such as lumphocytes, plasma cells, and macrophages in areas of demyelination, with evidence of phagocytosis of myelin and its breakdown products by macrophages. In contrast "inactive" lesions are hypocellular with scarring and loss of oligodendrocytes, the cells that produce myein. The presence of leukobytes in the CNS, where thay are normally absent, together with their early association with the demyelinating process, suggests that inflammation is involved in the pathogenesis of MS. Although the cause of MS is unknown, data from the published literature support immunologic or infectious factors leading to the state of chronic CNS inflammation. Migration of lymphocytes across the blood brain barrier and development of CNS inflammation is a hallmark of acute symptoms of multiple sclerosis. We will test the hypotheses that agents which interfere with the migration of cell by preventing adhesion of lymphocytes to capillary endothelium of the brain, will retard the inflammatory process and reduce or prevent the development of neurologic symptoms.

多发性硬化症是一种慢性疾病，其特征是由于中枢神经系统的物质损害而导致的神经功能障碍的反复发作。 MS病变随时间演变。 “活动性”病变在脱髓鞘区域中含有炎性细胞，如团块细胞、浆细胞和巨噬细胞，有证据表明巨噬细胞吞噬髓鞘及其分解产物。 相反，“非活性”病变是细胞减少，伴有瘢痕形成和少突胶质细胞（产生myein的细胞）的丢失。 白细胞在中枢神经系统中的存在，其中他们通常是缺席的，连同他们的早期协会与脱髓鞘过程，表明炎症参与MS的发病机制。虽然MS的原因是未知的，从已发表的文献数据支持免疫或感染因素导致的慢性CNS炎症的状态。淋巴细胞穿过血脑屏障的迁移和CNS炎症的发展是多发性硬化症急性症状的标志。 我们将检验这样的假设，即通过阻止淋巴细胞粘附到脑毛细血管内皮来干扰细胞迁移的药物将延缓炎症过程并减少或防止神经症状的发展。