Is Preterm Labor Influenced by the Maternal–Fetal Interface?

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
• pregnancy
• hyperplasia
• mPRα

Acknowledgments

This research was possible due to the assistance from the Office of Research Support, Faculty of Medicine, University of Coimbra, Portugal.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.