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

Emmet Hirsch, Yana Filipovich, Mala Mahendroo

Research output: Contribution to journalArticle

89 Scopus citations


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 (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). Results: Il1r1/Tnfrsf1a double-knockout mice had significantly lower rates of preterm delivery than controls (8% vs 69% with 7 × 107 bacteria, P = .002, and 52% vs 81% with 1.4 × 108 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.

Original languageEnglish (US)
Pages (from-to)1334-1340
Number of pages7
JournalAmerican journal of obstetrics and gynecology
Issue number5
StatePublished - May 1 2006


  • Infection
  • Interleukin 1
  • Mouse
  • Preterm labor
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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