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Can Carbon Monoxide Prevent Infection‐Mediated Preterm Birth in a Mouse Model?
Author(s) -
Peltier Morgan R.,
Koo HschiChi,
Gurzenda Ellen M.,
Arita Yuko,
Klimova Natalia G.,
Olgun Niccole,
Hanzeeh
Publication year - 2013
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12105
Subject(s) - proinflammatory cytokine , litter , placenta , offspring , pregnancy , amniotic fluid , medicine , cytokine , premature birth , inflammation , andrology , physiology , escherichia coli infection , immunology , gestation , escherichia coli , biology , fetus , biochemistry , genetics , gene , agronomy
Problem 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. Methods 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 E scherichia 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. Results 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. Conclusion 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.