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(Journal of Leukocyte Biology. 2000;68:693-699.)
© 2000 by Society for Leukocyte Biology

-Melanocyte-stimulating hormone peptides inhibit HIV-1 expression in chronically infected promonocytic U1 cells and in acutely infected monocytes

Wilma Barcellini^*, Gualtiero Colombo, Letteria La Maestra^*, Giuliana Clerici^*, Letizia Garofalo, Anna T. Brini, James M. Lipton and Anna Catania

Divisions of
^* Hematology and
Internal Medicine, Ospedale Maggiore di Milano IRCCS, 20122 Milano, Italy;
Department of Pharmacology, Chemotherapy, and Toxicology, University of Milan, 20133 Milano, Italy; and
Zengen, Inc., Woodland Hills, California

Correspondence: Anna Catania, III Divisione di Medicina Generale (Pad. Granelli), Ospedale Maggiore di Milano IRCCS, Via F. Sforza 35, 20122 Milano, Italy. E-mail: Anna.Catania{at}unimi.it

The purpose of the present research was to determine if -melanocyte-stimulating hormone (-MSH) and its C-terminal tripeptide [-MSH (11–13), KPV] alter HIV expression in infected cells. The results indicate that chronically HIV-1-infected promonocytic U1 cells produce -MSH and that immunoneutralization of the endogenous peptide enhances HIV expression. Because U1 cells express the -MSH receptor 1 (MC1R), an autocrine-inhibitory circuit based on the peptide and its receptor likely occurs in these cells. To determine effects of pharmacological concentrations of -MSH peptides on HIV expression, we measured p24 antigen release by TNF--stimulated U1 cells exposed to a wide range of concentrations of synthetic -MSH and KPV. Viral expression was reduced by both peptides. KPV also effectively reduced HIV replication in acutely infected monocyte-derived macrophages (MDM). The basis of the peptide influence on viral replication is at the transcriptional level; KPV inhibited activation of NF-B that is known to enhance viral expression. Endogenous -MSH likely contributes to natural defense against HIV. However, greater concentrations of synthetic peptide are much more effective in reducing HIV expression in infected cells.

Key Words: melanocortin peptides • melanocortin receptor 1 (MC1R) • nuclear factor B (NF-B)

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