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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2718-2726. Prepublished online as a Blood First Edition Paper on November 30, 2006; DOI 10.1182/blood-2006-03-012500. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-03-012500v1 109/7/2718    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Caselli, E. Articles by Santoro, M. G. Search for Related Content PubMed PubMed Citation Articles by Caselli, E. Articles by Santoro, M. G. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Chemokines, Cytokines, and Interleukins Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Human herpesvirus 8 acute infection of endothelial cells induces monocyte chemoattractant protein 1–dependent capillary-like structure formation: role of the IKK/NF-B pathway Elisabetta Caselli1, Simona Fiorentini2, Carla Amici3, Dario Di Luca1, Arnaldo Caruso2, and M. Gabriella Santoro3 1 Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy; 2 Department of Experimental and Applied Medicine, Section of Microbiology, University of Brescia, Italy; 3 Department of Biology, University of Rome Tor Vergata, Rome, Italy Human herpesvirus 8 (HHV-8) is considered the causative agent of Kaposi sarcoma, a highly vascularized neoplasm characterized by spindle-shaped cells of endothelial origin and inflammatory cell infiltration. The cell transforming ability of HHV-8 has been associated with the activation of NF-B, a nuclear factor playing a pivotal role in promoting inflammation and cell proliferation; however, little is known about NF-B activation during acute HHV-8 infection. In the present study, we used a recently established in vitro model of HHV-8 acute productive infection in endothelial cells to investigate the effect of HHV-8 on NF-B activity and function. HHV-8 rapidly and potently induced NF-B activity in endothelial cells via stimulation of the IB kinase (IKK). Following IKK activation, HHV-8 selectively triggered the production of high levels of monocyte chemoattractant protein 1 (MCP-1), whereas it did not affect the expression of other NF-B–dependent proinflammatory proteins, including TNF-, IL-8, and RANTES. Deletion of NF-B–binding sites in the MCP-1 enhancer resulted in significant inhibition of HHV-8–induced transcription. Furthermore, MCP-1 production was accompanied by virus-induced capillary-like structure formation at early stages of infection. The results suggest that HHV-8–induced MCP-1 may play an important role in promoting inflammation and pathogenic angiogenesis typical of HHV-8–associated lesions. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Totally tubular: virally induced endothelial tube formation Philip E. Pellett Blood 2007 109: 2669-2670. 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