Epidemiology of early pre-term delivery: relationship with clinical and histopathological infective parameters.

In this study, we want to evaluate which are the risk factors involved in early pre-term delivery (PTD). Spontaneous PTD results from two clinical conditions: (1) spontaneous pre-term labour (PTL) leading to PTD (idiopathic) and (2) pre-term premature rupture of membranes (pPROM). This is a multicentric, observational, retrospective, cross-sectional study, which includes 7,631 women admitted in the Obstetric units of Siena, Perugia, Torino, Trieste, Milano, Modena, Ancona, Foggia and Catania. Data were obtained from all patients having delivered spontaneously, pre-term or at term. The present study reveals the involvement of inflammation/infection in pathogenetic mechanisms leading to early PTD in the Italian population. A higher incidence of both clinical and pathological parameters of inflammation/infection - pPROM, genitourinary tract infections, placenta histopathological inflammation, WBC and C-reactive protein (CRP) - in early pre-term delivery in respect to late pre-term delivery and delivery at term, were shown.

Effects of urocortin 2 and urocortin 3 on IL-10 and TNF-α expression and secretion from human trophoblast explants.

OBJECTIVES: The aim of the present study was to evaluate the effect of Ucn2 and Ucn3 on cytokine expression and secretion from placental explants. STUDY DESIGN: Placentas were collected from healthy pregnancies at term elective caesarean delivery and trophoblast explants were prepared and treated with Ucn2 or Ucn3 in presence/absence of the selective CRH-R2 antagonist, astressin 2b. The mRNA expression and secretion of IL-10 and TNF-α were evaluated by Real Time RT-PCR and ELISA, respectively. MAIN OUTCOME MEASURES: To evaluate the possible role of Ucn2 and Ucn3 in inflammatory pathways. RESULTS: Ucn2 increased the mRNA expression and secretion of IL-10 and TNF-α, and Ucn3 increased the mRNA expression and secretion of IL-10, but did not modify the secretion of TNF-α. Ucn3 treatment reversed the LPS-induce increase of TNF-α expression and release, an effect blocked by astressin 2b. Ucn2 potentiated the LPS-induced increase of TNF-α expression and release, an effect reversed by astressin 2b. CONCLUSIONS: The present study showed that Ucn2 and Ucn3 differentially regulate the LPS-induced TNF-α and IL-10 expression and secretion in trophoblast explants acting through CRH-R2. A pro inflammatory effect of Ucn2 and an anti-inflammatory effect of Ucn3 in placental immunomodulatory mechanisms is suggested.