Send to:

Choose Destination
See comment in PubMed Commons below
Am J Obstet Gynecol. 2006 May;194(5):1334-40. Epub 2006 Apr 21.

Signaling via the type I IL-1 and TNF receptors is necessary for bacterially induced preterm labor in a murine model.

Author information

  • 1Department of Obstetrics, Evanston Northwestern Healthcare, Evanston, IL 60201, USA.



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.


Female mice lacking the type I receptors for IL-1 and TNF (Il1r1/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).


Il1r1/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.


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.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk