Is Preterm Labor Influenced by the Maternal-Fetal Interface?

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-beta, and membrane progesterone receptor alpha (mPR alpha) 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 mPR alpha and IL-10 in all layers, while Foxp3 expression occurred equally and only in the decidua. TGF-beta expression was similar in both groups. Preterm group placentas showed higher endothelial hyperplasia in both upper and lower halves of the placenta.