Abstract
OBJECTIVE: Cytomegalovirus infection causes adverse outcomes during pregnancy. Our objective was to determine the role of cytomegalovirus in modulating tumor necrosis factor (TNF)-related apoptosis-inducing ligand expression in the placenta.
STUDY DESIGN: TNF-related apoptosis-inducing ligand messenger RNA and protein were quantified in cytomegalovirus-infected placental fibroblasts by polymerase chain reaction and enzyme-linked immunosorbent assays, respectively. Blocking antibodies against interferon and type I interferon receptor were applied to culture medium to characterize the role of type I interferon in cytomegalovirus-induced TNF-related apoptosis-inducing ligand upregulation.
RESULTS: Expression of TNF-related apoptosis-inducing ligand messenger RNA and protein was increased in cytomegalovirus-infected placental fibroblasts, compared with uninfected controls. The cytomegalovirus-induced TNF-related apoptosis-inducing ligand messenger RNA upregulation was demonstrated across gestation, occurred in the absence of viral gene expression, and required cellular protein synthesis. TNF-related apoptosis-inducing ligand messenger RNA upregulation was markedly attenuated by inactivation of either type I interferon or its receptor.
CONCLUSION: One mechanism by which cytomegalovirus infection causes unfavorable pregnancy outcomes may involve placental upregulation of TNF-related apoptosis-inducing ligand via an interferon-mediated pathway.
Original language | English (US) |
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Pages (from-to) | 608.e1-608.e6 |
Journal | American journal of obstetrics and gynecology |
Volume | 197 |
Issue number | 6 |
DOIs | |
State | Published - Dec 2007 |
Keywords
- Cytomegalovirus Infections/immunology
- Female
- Humans
- Interferons/immunology
- Placenta/immunology
- Pregnancy
- TNF-Related Apoptosis-Inducing Ligand/biosynthesis
- Up-Regulation
- Virus Replication/immunology
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't
- Research Support, U.S. Gov't, Non-P.H.S.