Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 194, Issue 5, Pages 1334-1340Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2005.11.004
Keywords
interleukin 1; tumor necrosis factor; preterm labor; infection; mouse
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Funding
- NICHD NIH HHS [1R01HD41689] Funding Source: Medline
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Objective: We have shown previously that interleukin 1 (IL-1) signaling is not necessary for bacterially induced preterm delivery in mice. We now test whether combined signaling of IL-1 and tumor necrosis factor (TNF) is critical for this process. Study design: Female mice lacking the type I receptors for IL-1 and TNF (Illr1/Tnfrsf1a double-knockouts) and normal controls underwent intrauterine inoculation with killed Escherichia coli bacteria on day 14.5 of a 19- to 20-day gestation. Preterm delivery rates within 48 hours were recorded and gene expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Results: Illr1/Tnfrsf1a double-knockout mice had significantly lower rates of preterm delivery than controls (8% vs 69% with 7 x 10(7) bacteria, P = .002, and 52% vs 81% with 1.4 x 10(8) bacteria, P = .003) and significantly lower myometrial levels of cyclooxygenase (COX)-2. but not COX-1 mRNA. There were no genotype- or treatment-related differences in cervicovaginal and lower uterine expression of mRNAs for a variety of genes associated with cervical ripening. Conclusion: The combination of IL-1 and TNF signaling plays a critical role in bacterially induced labor and myometrial COX-2 production in the mouse. Cervical gene expression patterns during bacterially induced preterm labor suggest fundamental differences from spontaneous term labor in the cervical ripening process. (c) 2006 Mosby, Inc. All rights reserved.
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