These data indicate that Ccl-2 protein serves to integrate mechanical and endocrine signals contributing to uterine inflammation and the induction of labor and thus may represent a novel target for therapeutic prevention of preterm labor in humans.
A cross-sectional study was designed to examine the amniotic fluid concentrations of MCP-1 in women in two groups: 1) those presenting with preterm labor with intact membranes; and 2) those with preterm prelabor rupture of membranes (PROM).
Our preliminary results suggest that vaginal progesterone might prevent spontaneous preterm labor through a mechanism involving anti-inflammatory effects on UCFs, particularly suppression of IL-6 production.
Our findings suggest that the increased levels of TNF-alpha and CRH found in pregnant women presenting with preterm labor may be involved in the pathophysiological mechanism of the latter.
Placentas from pregnancies complicated by preterm PE had a significantly higher frequency of strong PAR-1 expression than placentas from women with spontaneous preterm labor.
Neurokinin B mRNA and protein are highly expressed in placenta at term and preterm labor; thus, the involvement of this neuropeptide in the events cascade leading to parturition may be suggested.
We investigated the role of genetic variation in the progesterone receptor (PGR) gene in modulating risks for preterm labor by examining both maternal and fetal effects.
Our findings suggest that the increased levels of TNF-alpha and CRH found in pregnant women presenting with preterm labor may be involved in the pathophysiological mechanism of the latter.
We conclude that protein levels of mPGES, as well as COX-2, can be stimulated by cytokines, potentially contributing to the increased prostaglandin production at the time of infection-driven preterm labor.