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This Article Full Text Full Text (PDF) 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 Thivierge, M. Articles by Rola-Pleszczynski, M. Search for Related Content PubMed PubMed Citation Articles by Thivierge, M. Articles by Rola-Pleszczynski, M. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Prostaglandin E2 Induces Resistance to Human Immunodeficiency Virus-1 Infection in Monocyte-Derived Macrophages: Downregulation of CCR5 Expression by Cyclic Adenosine Monophosphate Maryse Thivierge, Christian Le Gouill, Michel J. Tremblay, Jana Staková, and Marek Rola-Pleszczynski From the Groupe de Recherche en Immunologie, Département de Pédiatrie, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, Canada; and the Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec, Pavillon CHUL and Département de Biologie médicale, Faculté de Médecine, Université Laval, Ste-Foy, Canada. The chemokine receptor CCR5 can function as a coreceptor for human immunodeficiency virus-1 (HIV-1) entry into CD4+ T cells and macrophages, especially during the early stages of HIV-1 infection. The regulation of CCR5 expression may affect not only leukocyte migration, but also infectivity by HIV-1 and, therefore, acquired immunodeficiency syndrome (AIDS) pathogenesis. We report here that agents which increase intracellular concentrations of cyclic adenosine monophosphate (cAMP) rapidly downregulate CCR5 gene expression, with consequent loss of CCR5 expression and function in monocytes/macrophages. Chemotaxis and intracellular Ca2+ mobilization in monocytes pretreated with prostaglandin E2 or dibutyryl-cAMP for 24 hours were significantly reduced in response to the CCR5 ligand, MIP-1. Moreover, HIV-1 entry into monocyte-derived macrophages pretreated with dibutyryl-cAMP or prostaglandin E2 was markedly decreased. Our findings suggest that resistance to HIV-1 can be induced by agents which increase cellular levels of cAMP and that this may suggest additional therapeutic strategies to limit infection by HIV-1. Blood, Vol. 92 No. 1 (July 1), 1998: pp. 40-45 © 1998 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Moriuchi and H. Moriuchi Induction of Lactoferrin Gene Expression in Myeloid or Mammary Gland Cells by Human T-Cell Leukemia Virus Type 1 (HTLV-1) Tax: Implications for Milk-Borne Transmission of HTLV-1 J. Virol., July 15, 2006; 80(14): 7118 - 7126. 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