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pubmed-article:7668162pubmed:abstractTextOpioid peptides appear to have an immunomodulatory activity. Using the chronically HIV-1-infected promonocyte clone U1, we investigated the effect of endogenous and synthetic opioid agonists on cytokine-induced HIV-1 expression. None of the endogenous or synthetic opioid agonists had an effect on constitutive HIV-1 expression. Opioid agonists such as methionine-enkephalin, dynorphin, and the kappa receptor agonist, U50,488, dose-dependently suppressed (> 40%) interleukin (IL)-6-induced upregulation of HIV-1 expression. Interestingly, opioid receptor antagonists (mu, delta, and kappa types) also inhibited (> 60%) IL-6-induced upregulation of HIV-1 expression. All opioid agonists and antagonists tested only modestly suppressed (< 20%) tumor necrosis factor-alpha-induced upregulation of HIV-1 expression in U1 cell cultures. These data suggest that certain opioid peptides alter an IL-6-induced signal transduction pathway which triggers HIV-1 expression in the chronically infected promonocyte U1.lld:pubmed
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pubmed-article:7668162pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:7668162pubmed:articleTitleEndogenous opioid peptides suppress cytokine-mediated upregulation of HIV-1 expression in the chronically infected promonocyte clone U1.lld:pubmed
pubmed-article:7668162pubmed:affiliationNeuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, MN 55404, USA.lld:pubmed
pubmed-article:7668162pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7668162pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed