RT Journal Article SR Electronic T1 Impact of Mediators Present in Amniotic Fluid on Preterm Labour JF In Vivo JO In Vivo FD International Institute of Anticancer Research SP 799 OP 812 VO 26 IS 5 A1 NIKOLAOS VRACHNIS A1 STAMATIOS KARAVOLOS A1 ZOE ILIODROMITI A1 STAVROS SIFAKIS A1 CHARALAMBOS SIRISTATIDIS A1 GEORGE MASTORAKOS A1 GEORGE CREATSAS YR 2012 UL http://iv.iiarjournals.org/content/26/5/799.abstract AB Preterm birth continues to be one of the most important issues in current obstetric medicine, being the single largest cause of perinatal morbidity and mortality. The signals that initiate preterm and term labour remain a mystery. Intrauterine inflammation with the secretion of cytokines is one of the accepted explanations for the mechanism of initiation of preterm labour. This review discusses the current understanding of the molecular mechanisms for the initiation of preterm labour, focusing chiefly on the role of intra-amniotic fluid mediators, whether endogenous or infection-induced, in the regulation of inflammatory response pathways associated with spontaneous preterm labour. Prostaglandins (PGs) are considered to be one of the key mediators of preterm labour, with the concentration of biologically active PGs in the amniotic fluid, particularly PGE2 and PGF2α, being significantly higher in women with preterm labour. Cytokines, such as interleukins and tumour necrosis factor alpha, additionally play a dominant role in preterm labour, particularly in association with infection. Elevated amniotic fluid concentrations of extracellular matrix mediators, including metalloproteases, are also implicated in the process of foetal membrane rupture in preterm labour. Allelic variations in the main amniotic fluid mediators may be the key to understanding the disparity in the rates of preterm birth between different ethnic populations. We also discuss the role of other potential mediators such as cell-adhesion molecules, nitric oxide and novel biomarkers found in the amniotic fluid.