Premium
Induction of cyclooxygenase‐2 expression during HIV‐1‐infected monocyte‐derived macrophage and human brain microvascular endothelial cell interactions
Author(s) -
Pereira Cândida F.,
Boven Leonie A.,
Middel Jeena,
Verhoef Jan,
Nottet Hans S. L. M.
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.3.423
Subject(s) - biology , inflammation , monocyte , endothelium , macrophage , cyclooxygenase , immunology , cell type , microglia , endothelial stem cell , microbiology and biotechnology , neuroinflammation , cell , in vitro , cancer research , enzyme , endocrinology , biochemistry , genetics
Human immunodeficiency virus type‐1 (HIV‐1)‐associated dementia (HAD) is a neurodegenerative disease characterized by HIV infection and replication in brain tissue. HIV‐1‐infected monocytes overexpress inflammatory molecules that facilitate their entry into the brain. Prostanoids are lipid mediators of inflammation that result from cyclooxygenase‐2 (COX‐2) activity. Because COX‐2 is normally induced during inflammatory processes, the aim of this study was to investigate whether COX‐2 expression is up‐regulated during monocyte‐brain endothelium interactions. In vitro cocultures of HIV‐infected macrophages and brain endothelium showed an up‐regulation of COX‐2 expression by both cell types. This up‐regulation occurs via an interleukin‐1β (IL‐1β)‐dependent mechanism in macrophages and via an IL‐1β‐independent mechanism in endothelial cells. Thus, interactions between HIV‐infected monocytes and brain endothelium result in COX‐2 expression and, as such, might contribute to the neuropathogenesis of HIV infection.