Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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AIDS Dementia Complex / metabolism
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AIDS Dementia Complex / pathology
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AIDS Dementia Complex / virology*
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Adult
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Antibodies / pharmacology
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Brain / blood supply
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Brain / pathology
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Brain / virology*
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CD4 Antigens / genetics
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CD4 Antigens / immunology
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CD4 Antigens / metabolism*
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Cell Movement / immunology
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Child
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Child, Preschool
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Endothelium, Vascular / chemistry
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Endothelium, Vascular / metabolism
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Endothelium, Vascular / virology*
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Flow Cytometry
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Frozen Sections
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HIV Envelope Protein gp120 / immunology
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HIV Envelope Protein gp120 / metabolism*
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HIV-1*
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Humans
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In Vitro Techniques
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Intercellular Adhesion Molecule-1 / analysis
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Intercellular Adhesion Molecule-1 / biosynthesis
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Monocytes / cytology
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Monocytes / immunology
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Monocytes / virology
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RNA, Messenger / analysis
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Vascular Cell Adhesion Molecule-1 / analysis
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Vascular Cell Adhesion Molecule-1 / biosynthesis
Substances
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Antibodies
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CD4 Antigens
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HIV Envelope Protein gp120
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RNA, Messenger
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Vascular Cell Adhesion Molecule-1
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Intercellular Adhesion Molecule-1