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Fetal immune response to oral pathogens and risk of preterm birth

Kim A Boggess1, Kevin Moss, Phoebus Madianos

  • 1Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of North Carolina School of Medicine, Chapel Hill 27599-7516, USA. kboggess@med.unc.edu

American Journal of Obstetrics and Gynecology
|September 15, 2005
PubMed

Insights

Fetal immune responses to oral pathogens, indicated by immunoglobulin M (IgM) antibodies, are linked to preterm birth. The risk is amplified when fetuses also show signs of inflammation.

Area of Science:

  • Obstetrics and Gynecology
  • Immunology
  • Neonatal Research

Background:

  • Preterm birth remains a leading cause of neonatal morbidity and mortality.
  • The role of fetal inflammatory and immune responses in the etiology of preterm birth requires further elucidation.

Purpose of the Study:

  • To investigate the association between fetal inflammatory markers and immune responses to oral pathogens and the risk of preterm birth.

Main Methods:

  • Prospective collection of 640 umbilical cord blood samples.
  • Measurement of inflammatory mediators (C-reactive protein, IL-1beta, IL-6, TNF-alpha, Prostaglandin E2, 8-isoprostane) and fetal IgM antibodies to oral pathogens.
  • Statistical analysis to determine the relationship between these markers and spontaneous preterm birth (<35 weeks).

Main Results:

  • Preterm birth rates were significantly higher in cases with elevated 8-isoprostane or TNF-alpha levels, and with positive fetal IgM response to oral pathogens.
  • Combined fetal IgM seropositivity with elevated C-reactive protein, 8-isoprostane, Prostaglandin E2, or TNF-alpha significantly increased the adjusted odds ratio for preterm birth.

Conclusions:

  • Fetal exposure to oral pathogens, evidenced by an IgM response, is associated with an increased risk of preterm birth.
  • The risk is substantially elevated when fetal inflammation is also present, highlighting a dual immune and inflammatory pathway.
Abstract

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