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Intraperitoneal infusion of proinflammatory cytokines does not cause activation of the rat uterus during late gestation

Perinatal Research Centre, Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Canada

Submitted 10 February 2005 ; accepted in final form 22 April 2005

Increased concentrations of IL-1 and TNF- have been associated with parturition. However, the role of these cytokines is unknown. Before parturition, the uterus undergoes a process of activation, during which there are significant changes in expression of genes associated with increased uterine contractility, including the receptors for oxytocin (OT) and prostaglandin (PG)F₂ (FP), PGH₂ synthase isoform 2 (PGHS2), the gap junction protein connexin-43 (Cx-43), and the inducible isoform of nitric oxide synthase (iNOS). To determine whether IL-1 or TNF- was part of the causal mechanism for increased uterine contractions, we placed osmotic pumps infusing IL-1 or TNF- into the peritoneal cavity of late pregnant rats (gestation day 19) and measured the effects on uterine contractility and on the uterine concentrations of mRNA for the contraction-associated genes 24 h later. Maternal serum concentrations of IL-1 and TNF- were increased significantly. By day 21, the control animals had significant increases (P 0.05) in mRNA for OT, FP, PGHS2, and Cx-43, a decrease (P 0.05) in iNOS, and an increase (P 0.05) in uterine sensitivity and responsiveness to OT. Infusion of IL-1 or TNF- had no effect on uterine contractility or on expression of the activation-associated genes. We conclude that intraperitoneal infusion of IL-1 or TNF- resulting in significantly increased maternal serum cytokine levels does not cause uterine activation. The role of proinflammatory cytokines in the mechanism of parturition remains unclear.

interleukin-1; tumor necrosis factor-; contraction-associated proteins; uterine contractility; parturition