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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.
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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.
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