Stins M F, Shen Y, Huang S H, Gilles F, Kalra V K, Kim K S
Division of Infectious Diseases, Childrens Hospital Los Angeles, California, USA.
J Neurovirol. 2001 Apr;7(2):125-34. doi: 10.1080/13550280152058780.
Encephalopathy represents a common and serious manifestation of HIV-1 infection in children, but its pathogenesis is unclear. We demonstrated that gp120 activated human brain microvascular endothelial cells (HBMEC) derived from children in up-regulating ICAM-1 and VCAM-1 expression, IL-6 secretion and increased monocyte transmigration across monolayers. Another novel observation was our demonstration of CD4 in isolated HBMEC and on microvessels of children's brain cryosections. Gp120-induced monocyte migration was inhibited by anti-gp120 and anti-CD4 antibodies. This is the first demonstration that gp120 activates HBMEC via CD4, which may contribute to the development of HIV-1 encephalopathy in children.
脑病是儿童HIV-1感染常见且严重的表现，但发病机制尚不清楚。我们证明，gp120可上调儿童来源的人脑微血管内皮细胞（HBMEC）中细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）的表达、白细胞介素-6（IL-6）的分泌，并增加单核细胞穿过单层细胞的迁移。另一个新发现是，我们在分离的HBMEC以及儿童脑冰冻切片的微血管上发现了CD4。抗gp120和抗CD4抗体可抑制gp120诱导的单核细胞迁移。这首次证明gp120通过CD4激活HBMEC，这可能有助于儿童HIV-1脑病的发展。
