Molecular analysis of endometrial inflammation in preterm birth

Abstract

Spontaneous preterm birth (sPTB) represents the 35%-45% of all preterm birth (PTB) cases and its etiology is unknown. We investigated if the expression level of endometrial cytokines and angiogenetic factors is related to the onset of sPTB.Endometrial tissues from non-pregnant women who experienced sPTB and from non-pregnant women who did not experience sPTB were collected and examined for their expression profile. With this aim, the PCR Array analysis was performed and data were confirmed by Real-Time PCR. Differential gene expression measurements (pathological vs control tissues) showed a significant up-regulation for genes codifying for two angiogenetic factors known as connective tissue growth factor (CTGF), and coagulation factor III (F3). An increased level of expression was detected both for tyrosine kinase endothelial (TEK) and for transforming growth factor beta 2 (TGF-β2) genes but without reaching the statistical significance. The expression level of interleukin 10 receptor alpha (IL10RA) gene was slightly decreased in pathological group compared to control one but, as well as forTEK and TGF-β2 measurements, without reaching the statistical significance. Our work is the first to correlate the imbalance in endometrial district of non -pregnant women with sPTB. These data could suggest a new point of view whence to read sPTB. We need additional clinical and biological studies to clarify sPTB pathogenesis.

Cytokine profiling: variation in immune modulation with preterm birth vs. uncomplicated term birth identifies pivotal signals in pathogenesis of preterm birth

“…Cecati et al. demonstrated that the IL-10 receptors were downregulated in the endometrium in a group of women recently delivering preterm when compared to non-pregnant women (experiencing term birth) by endometrial biopsy [ 28 ]. Hence, the demonstration of IL-10 decrease in our cohort of preterm deliveries again points toward IL-10’s importance in achieving term gestational age.…”

“…Prior data has demonstrated progesterone withdrawal to have effects on cells with progesterone receptors, leading to cytokine upregulation, increase in local inflammation and enzymes responsible for tissue breakdown as well as vasoconstriction. Cytokine release within the myometrium has been shown to effect matrix metalloproteinase activity that has been demonstrated to lead to cervical modeling with decrease in cervical stroma and in effect cervical shortening as well as weakening of the amniotic and chorionic membranes thereby priming the gestation for labor whether preterm or term [ 27 ], [ 28 ]…”

Something Smells Fishy: How Lipid Mediators Impact the Maternal–Fetal Interface and Neonatal Development

“…Intrauterine inflammation can be due to microbes or sterile intra-amniotic inflammation that can occur without the presence of a pathological infection. Sterile inflammation is significantly greater for women with preterm labor and intact membranes [88], while endometrial inflammation can also be a causative factor in preterm labor [89]. This could be due to other alarm signals within the intrauterine environment, which activate intracellular pathways leading to the same cytokine mediators as an infection [90].…”

The Role of Kisspeptin in the Pathogenesis of Pregnancy Complications: A Narrative Review

“…Oxytocin is one of the most crucial hormones in parturition, mainly due to inducing uterine contraction [ 131 ]. It is worth underlying that endometrial inflammation, reflected by an increase in inflammatory markers including endometrial cytokines and angiogenetic factors, has been found to play a pivotal role in the pathogenesis of preterm delivery [ 132 ]. However, some authors have indicated that oxytocin exerts different effects after degradation to active fragments, and its anti-inflammatory properties are postulated [ 133 ].…”