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.
- Human cerebral microvessel endothelium
- Transendothelial migration of monocytes
ASJC Scopus subject areas
- Clinical Neurology
- Cellular and Molecular Neuroscience