Expression of adhesion molecules and monocyte chemoattractant protein-1 (MCP-1) in the spinal cord lesions in HTLV-I-associated myelopathy
Expression of adhesion molecules and monocyte chemoattractant protein-1 (MCP-1) in the spinal cord lesions in HTLV-I-associated myelopathy
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DOI：
10.1007/s004010050435
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发表时间：
1996-04-01
影响因子：
12.7
通讯作者：
Osame, M
中科院分区：
文献类型：
--
作者：
Umehara, F;Izumo, S;Osame, M
白细胞与内皮细胞的粘附分子在炎症性疾病的发病机制中起重要作用，包括HTLV-I相关的脊髓病（HAM）/热带痉挛性下肢轻瘫（TSP）。为了帮助确定粘附分子在HAM/TSP中的作用，我们研究了淋巴细胞功能相关抗原-1（LFA-1）、Mac-1、极晚期抗原-4（VLA-4）、唾液酸刘易斯（x）（SLex）、细胞间粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）、内皮细胞粘附分子-1（ELAM-1）和单核细胞趋化蛋白-1（MCP-1）在HAM/TSP脊髓病变中的表达。结果表明，HAM/TSP脊髓损伤组内皮细胞VCAM-1表达明显高于对照组。浸润的单个核细胞，特别是血管周围病变，表达VLA-4。HAM/TSP组脊髓中ICAM-1的表达与对照组无显著性差异，但HAM/TSP组脊髓中浸润的单核细胞强烈表达LFA-1和Mac-1。ELAM-1在5个HAM/TSP中的3个的非活动性慢性病变的内皮上表达，但在对照组的脊髓中未检测到。HAM/TSP组脊髓血管周围细胞偶见SLex反应，而对照组未见。MCP-1在活动性-慢性病变的血管周围浸润细胞和血管内皮细胞上可检测到。本研究提示VLA-4/VCAM-1相互作用可能在淋巴细胞向中枢神经系统（CNS）迁移中起重要作用，MCP-1也可能参与HAM/TSP中炎性细胞向CNS的募集。
Leukocyte adhesion molecules to endothelium plays an important role in the pathogenesis of inflammatory diseases, including HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). To help define the role of adhesion molecules in HAM/TSP, we studied the expression of lymphocyte function-associated antigen-1 (LFA-1), Mac-1, very late antigen-4 (VLA-4), Sialyl Lewis(x) (SLex), intercelluar adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1) and monocyte chemoattractant protein-1 (MCP-1) in the spinal cord lesions of HAM/TSP. The results indicate that spinal cord lesions of HAM/TSP have greater VCAM-1 expression on endothelium compared with those of controls. Infiltrating mononuclear cells, especially perivascular lesions, expressed VLA-4. Although the expression of ICAM-1 in the spinal cords was not distinctive between HAM/TSP and controls, infiltrating mononulcear cells in the spinal cords of HAM/TSP strongly expressed LFA-1 and Mac-1. ELAM-1 was expressed on endothelium in the inactive-chronic lesions from three of five HAM/TSP, but was not detectable in the spinal cords of controls. SLex reaction was detectable on occasional perivascular cells in the spinal cord of HAM/TSP, but not in those of controls. MCP-1 was detectable on perivascular infiltrating cells and vascular endothelium in active-chronic lesions. This study suggests that VLA-4/VCAM-1 interaction may play an important role for lymphocyte migration into the central nervous system (CNS), and MCP-1 may also be in volved in inflammatory cell recruitment to the CNS in HAM/TSP.