Journal
REPRODUCTIVE SCIENCES
Volume 26, Issue 4, Pages 551-559Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719118804420
Keywords
preterm birth; cervical remodeling; inflammation
Categories
Funding
- Department of Women's Health at Hartford Hospital
- NIH [HD054931]
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Objective: A multitude of factors promotes inflammation in the reproductive tract leading to preterm birth. Macrophages peak in the cervix prior to birth and their numbers are increased by the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF). We hypothesize GM-CSF is produced from multiple sites in the genital tract and is a key mediator in preterm birth. Study Design: Ectocervical, endocervical, and amniotic fluid mesenchymal stem cells were treated with lipopolysaccharide (LPS), and the concentration and expression of GM-CSF was measured. Pregnant CD-1 mice on gestational day 17 received LPS and an intravenous injection of either anti-mouse GM-CSF or control antibody. After 6 hours, the preterm birth rate was recorded. Results: Treatment with LPS increased the GM-CSF concentration and messenger RNA expression after 24 hours in all 3 cell lines (P < .01). Mice treated with LPS and the GM-CSF antibody had a preterm birth rate of 25%, compared to a 66.7% preterm birth rate in controls, within 6 hours (P < .05, chi(2)). Treatment with the anti-mouse GM-CSF antibody decreased the concentration of GM-CSF in the mouse serum (P < .01) but did not alter the number of macrophages or collagen content in the cervix. Conclusion: These studies demonstrate that GM-CSF is produced from multiple sites in the genital tract and that treatment with an antibody to GM-CSF prevents preterm birth. Curiously, the anti-mouse GM-CSF antibody did not decrease the number of macrophages in the cervix. Further research is needed to determine whether antibodies to GM-CSF can be utilized as a therapeutic agent to prevent preterm birth.
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