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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/23637
Title: Down Modulation of TNF-α mRNA Placental Expression by AZT Used for the Prevention of HIV-1 Mother-to-Child Transmission
Authors: S. Pornprasert
A. Faye
J. Y. Mary
G. Dolcini
P. Leechanachai
G. Chaouat
N. Ngo
F. Barré-Sinoussi
E. Menu
Chiang Mai University
Institut Pasteur, Paris
Mahidol University
Inserm
Universite Paris 7- Denis Diderot
Keywords: Medicine
Issue Date: 1-Sep-2006
Citation: Placenta. Vol.27, No.9-10 (2006), 989-995
Abstract: Mechanisms of HIV-1 in utero mother-to-child transmission (MTCT) protection provided by AZT are not completely understood. The placental cytokine network is involved in the control of HIV-1 in utero transmission but the effect of AZT on this network is unknown. To evaluate the effects of AZT on placental cytokine expression, the chorionic villi from HIV-1 uninfected women term placentae were cultured with 0, 100, and 2000 ng/ml AZT. Tissue fragments were harvested at days 1, 4, and 7 to determine the level of cytokine mRNA by real-time RT-PCR. The viability and morphology of the placental histocultures were monitored by the expression of beta-human chorionic gonadotropin (β-hCG) gene, lipopolysaccharide (LPS) activation, and microscopic examination. AZT at 2000 ng/ml significantly down-regulated TNF-α mRNA expression at day 1 and day 4, but had no effect on β-hCG, stromal cell-derived factor 1 (SDF-1), and IL-10 gene expression. AZT did not induce any deleterious impact on placental tissue structure. Furthermore, activation of chorionic villi by LPS for 24 h up-regulated IL-10 and TNF-α mRNA expression. Down-regulation of TNF-α mRNA could represent a mechanism through which AZT can decrease the risk of HIV-1 MTCT, in addition to its direct effect on HIV-1 replication. © 2005 Elsevier Ltd. All rights reserved.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=33747155554&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/23637
ISSN: 01434004
Appears in Collections:Scopus 2006-2010

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