title: PGJ2 antagonizes NF-kappaB-induced HIV-1 LTR activation in colonic epithelial cells.
abstract: Intestinal epithelial cells play an important role in early stages of HIV-1 infection and long-term persistence of the virus. Here we determined the mechanism that regulates HIV-1 activation via prostaglandin J(2) (PGJ(2)) in Caco-2 cells. We showed that treatment of Caco-2 cells with PGJ(2) decreased the infectivity of a luciferase reporter virus, pHXB-luc, as well as HIV production following infection of cells with a X4-tropic virus by antagonizing sodium butyrate, a cellular activator known to induce HIV-1 transcription. Transfection of intestinal epithelial cells such as Caco-2, HT-29 and SW620 cells with full-length HIV-1 LTR (pLTR-luc) revealed that PGJ(2) reduced HIV-1 LTR-mediated reporter gene activity. The involvement of NF-kappaB in the PGJ(2)-dependent down-regulation of HIV-1 transcription was further assessed using the kappaB-regulated luciferase-encoding vectors. In Caco-2 cells, PGJ(2) decreased IKK activity, resulting in reduced NF-kappaB translocation to the nucleus. Since sodium butyrate has been associated with a chronic stress response in AIDS patients, our results suggest that addition of PGJ(2) in the environment of infected intestinal epithelial cells could reduce HIV-1 transcription.
authors.affiliation: Département de Biologie, Faculté des Sciences, Université de Sherbrooke, 2500 Boul de l'Université Sherbrooke, QC, Canada.
authors.forename: Mélissa
authors.initials: M
authors.lastname: Boisvert
authors.forename: Sandra
authors.initials: S
authors.lastname: Côté
authors.forename: Amandine
authors.initials: A
authors.lastname: Vargas
authors.forename: Stamatoula
authors.initials: S
authors.lastname: Pasvanis
authors.forename: Salim
authors.initials: S
authors.lastname: Bounou
authors.forename: Benoit
authors.initials: B
authors.lastname: Barbeau
authors.forename: Nancy
authors.initials: N
authors.lastname: Dumais