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Effect of Carbon Monoxide on Bacteria-Stimulated Cytokine Production by Placental Explants

Authors

  • Morgan R. Peltier,

    1. Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
    2. Department of Obstetrics and Gynecology, Winthrop University Hospital, Mineola, NY, USA
    3. Department of Obstetrics, Gynecology and Reproductive Medicine, SUNY-Stony Brook, Stony Brook, NY, USA
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    • These authors contributed equally to this paper.

  • Yuko Arita,

    1. Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
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    • These authors contributed equally to this paper.

  • Ellen M. Gurzenda,

    1. Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
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  • Natalia Klimova,

    1. Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
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  • Hschi-Chi Koo,

    1. Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
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  • Amitasrigowri Murthy,

    1. Department of Obstetrics and Gynecology, Bellevieu Hospital, New York, NY, USA
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  • Nazeeh Hanna

    Corresponding author
    1. Department of Pediatrics, Winthrop University Hospital, Mineola, NY, USA
    • Women's and Children's Research Laboratory, Winthrop University Hospital, Mineola, NY, USA
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Correspondence

Nazeeh Hanna, Department of Pediatrics, Winthrop University Hospital, 259 First Street, Mineola, NY, USA 11501.

E-mail: nhanna@winthrop.org

Abstract

Problem

Preterm birth is frequently caused by an inflammatory response to ascending infections of the reproductive tract. Carbon monoxide (CO) has potent anti-inflammatory properties at subtoxic concentrations. Whether or not CO can modulate inflammatory responses by placental tissues is unclear.

Methods

Placental explant cultures were incubated with heat-killed Escherichia coli or Ureaplasma parvum in the presence or absence of 250 ppm CO for 24 hr. Concentrations of cytokines relative viability of the cultures were quantified.

Results

Escherichia coli- and U. parvum-stimulated IL-1β production was significantly inhibited by CO supplementation. Escherichia coli-stimulated, but not U. parvum-stimulated, IFN-γ production was inhibited by CO. While CO inhibited PGE2 production by unstimulated cells, no effects on bacteria-stimulated prostaglandin production were detected. CO had no effect on basal or E. coli-stimulated TNF-α production but enhanced TNF-α production by cultures stimulated with U. parvum. In addition, CO tended to improve the viability of the placental cultures.

Conclusions

Low concentrations of CO tended to reduce proinflammatory cytokines and to promote the production of anti-inflammatory cytokines in a pathogen-specific manner. These properties suggest that CO may be useful for promoting a pro-pregnancy cytokine milieu by placental explants and may reduce the consequences of intrauterine infections.

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