Is Preterm Labor Influenced by the Maternal-Fetal Interface?

Fetal Pediatr Pathol. 2017 Apr;36(2):89-105. doi: 10.1080/15513815.2016.1242674. Epub 2016 Nov 9.

Abstract

Preterm labor (PTL) accounts for almost 11% of deliveries, and is a major cause of neonatal morbidity and mortality. T regulatory (Treg) cells may prevent fetal rejection by the maternal immune system under the influence of progesterone. Case control study was conducted to determine Treg cells, IL-10, TGF-β, and membrane progesterone receptorα (mPRα) in the maternal-fetal interface (placenta), including eight pregnant women with threatened PTL (study group) and 16 normal-delivery women (control group). Comparing study group versus control, mean gestational age of delivery differed significantly (p = 0.02), as did endothelial hyperplasia in the upper half (p = 0.035) and the lower half (p = 0.005) of the placenta. Besides, there was higher expression of mPRα and IL-10 in all layers, while Foxp3 expression occurred equally and only in the decidua. TGF-β expression was similar in both groups. Preterm group placentas showed higher endothelial hyperplasia in both upper and lower halves of the placenta.

Keywords: Placental disorder; hyperplasia; mPRα; pregnancy.

MeSH terms

  • Adult
  • Case-Control Studies
  • Female
  • Fetal Development / physiology*
  • Fetus*
  • Gestational Age
  • Humans
  • Infant, Newborn
  • Maternal-Fetal Relations
  • Obstetric Labor, Premature / physiopathology*
  • Placenta / physiopathology*
  • Pregnancy
  • Premature Birth / etiology*
  • Transforming Growth Factor beta / metabolism

Substances

  • Transforming Growth Factor beta