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(Journal of Leukocyte Biology. 2000;68:423-428.)
© 2000 by Society for Leukocyte Biology

Induction of cyclooxygenase-2 expression during HIV-1-infected monocyte-derived macrophage and human brain microvascular endothelial cell interactions

Cândida F. Pereira, Leonie A. Boven, Jeena Middel, Jan Verhoef and Hans S. L. M. Nottet

Eijkman-Winkler Institute for Microbiology, Infectious Diseases and Inflammation, University Medical Center, Utrecht, The Netherlands

Correspondence: Cândida da Fonseca Pereira, Eijkman-Winkler Institute, Section Neuroimmunology, UMC, hp G04.614, Heidelberglaan 100, NL-3584 CX Utrecht, The Netherlands. E-mail: C.F.Pereira{at}lab.azu.nl

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-1ß (IL-1ß)-dependent mechanism in macrophages and via an IL-1ß-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.

Key Words: HIV-1-associated dementia • cytokines • eicosanoids • in vitro cocultures • reverse transcriptase-polymerase chain reaction • Western blot




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