These authors contributed equally to this paper.
Can Carbon Monoxide Prevent Infection-Mediated Preterm Birth in a Mouse Model?
Article first published online: 26 MAR 2013
© 2013 John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 70, Issue 1, pages 31–37, July 2013
How to Cite
Can carbon monoxide prevent infection-mediated preterm birth in a mouse model? Am J Reprod Immunol 2013; 70: 31–37., , , , , , .
- Issue published online: 11 JUN 2013
- Article first published online: 26 MAR 2013
- Manuscript Accepted: 29 JAN 2013
- Manuscript Received: 4 DEC 2012
- Prematurity Research Initiative Program. Grant Number: #21-FY11-4
- preterm birth
Preterm birth is frequently caused by intrauterine infection and inflammation. Recent studies have demonstrated that carbon monoxide (CO), which is produced endogenously, has potent anti-inflammatory properties. Whether or not CO can prevent infection-mediated preterm birth is unknown.
Mice were assigned to one of four groups: sham infection, sham infection + CO, infection, or infection + CO. Infections were established by intra-uterine injection of Escherichia coli on day 14 of pregnancy. Animals received daily i.p. injections of 1 mL CO-saturated lactated ringers solution (LRS) or LRS alone beginning on the morning of surgery. Gestational age at delivery and litter characteristics was noted. In second experiment, animals were sacrificed 24 hrs post-surgery and tissues were harvested for cytokine analyses.
Escherichia coli intrauterine infection increased the number of animals delivering preterm. This effect was significantly ameliorated by CO-LRS. CO-treatment also increased litter size and weights of the surviving offspring. Cytokines in the amniotic fluid and the placenta were increased by E. coli exposure, but CO had no detectible effect on E. coli-stimulated cytokine production. No effects of CO were detected in sham-infected animals.
Supplemental CO improves pregnancy outcome after intrauterine infection and may function at a point downstream of, or through pathways independent of, induction of proinflammatory cytokines.