Bacterially induced preterm labor in the mouse does not require maternal interleukin-1 signaling

Am J Obstet Gynecol. 2002 Mar;186(3):523-30. doi: 10.1067/mob.2002.120278.


Objective: We tested the hypothesis that intrauterine bacterial inoculation induces labor via expression of the inflammatory cytokine interleukin-1 (IL-1) in a murine model.

Study design: Pregnant mice on day 14.5 of a 19-20 day gestation were inoculated with killed Escherichia coli or sterile media into either (a) the right uterine horn, (b) the right uterine horn following its surgical isolation from the contralateral horn and cervix, or (c) the kidney. Cytokine levels in gestational tissues and maternal serum were determined by use of enzyme-linked immunosorbent assay (ELISA). In a separate experiment, bacterially induced preterm delivery was compared between mice lacking a functional IL-1 receptor and wild-type control litter mates.

Results: Killed E coli induced delivery within 48 hours with similar dose-response curves regardless of inoculation site (intact uterine horn, isolated uterine horn, or kidney). Bacterial inoculation of an isolated right horn caused dramatic increases in local expression of IL-1 and IL-6. However, delivery occurred from the uninjected horn without corresponding upregulation of cytokines, with the exception of a modest rise within fetal membranes. Mice lacking a functional IL-1 receptor were no different from wild-type mice in their susceptibility to bacterially induced delivery.

Conclusion: Bacterially induced labor in the murine model does not require IL-1 signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Escherichia coli Infections / complications*
  • Female
  • Inflammation Mediators / metabolism
  • Interleukin-1 / physiology*
  • Mice
  • Mice, Knockout / genetics
  • Obstetric Labor, Premature / microbiology*
  • Pregnancy
  • Pregnancy, Animal / physiology*
  • Receptors, Interleukin-1 / deficiency
  • Receptors, Interleukin-1 / genetics
  • Signal Transduction / physiology*
  • Uterus / metabolism


  • Cytokines
  • Inflammation Mediators
  • Interleukin-1
  • Receptors, Interleukin-1