K. Shimoya

Fetal mononuclear cells show a comparable capacity with maternal mononuclear cells to produce IL-8 in response to lipopolysaccharide in chorioamnionitis

IL-8 is a chemotactic and activating cytokine for neutrophils which eliminate invading bacteria by releasing bactericidal metabolites. Cord blood mononuclear cells (CBMCs) obtained from neonates born to mothers with chorioamnionitis actively produced a significantly higher amount of IL-8 than those of neonates without chorioamnionitis, suggesting that the mononuclear cells of fetuses with chorioamnionitis had been activated in utero. As lipopolysaccharide (LPS) can often be detected in the uteroplacental space in chorioamnionitis, the LPS-mediated activation mechanism of neonatal mononuclear cells was analyzed in vitro to produce IL-8. Neonatal mononuclear cells stimulated with LPS increased IL-8 production in a time- and dose-dependent manner. The ability of term or preterm neonatal mononuclear cells to produce IL-8 was comparable with that of adult (maternal) mononuclear cells, suggesting functional maturity of the neonatal or fetal mononuclear cells to produce IL-8. However, IL-8 production by neonatal CBMCs was down-regulated by dexamethasone, a glucocorticoid which is clinically administered to mothers to promote fetal lung maturity in preterm delivery. Our present study revealed a regulatory mechanism of fetal IL-8 production, suggesting that functionally mature fetal mononuclear cells produce IL-8 in response to LPS in chorioamnionitis and activate the fetal defense mechanism against infection.

Interleukin-8 level in maternal serum as a marker for screening of histological chorioamnionitis at term.

Objective: To establish a clinical method for immediate diagnosis of histological chorioamnionitis, by maternal blood sampling at term. Method: The sera of 22 mothers with chorioamnionitis and 81 mothers without chorioamnionitis at term delivery were collected. The serum levels of cytokines including interleukin‐1α (IL‐1α), interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8) were titered and other conventional markers such as white blood cell and CRP were measured simultaneously. Chorioamnionitis was histopathologically confirmed after delivery. Result: The sera of mothers with histological chorioamnionitis showed a significant increase in IL‐8 titer, but not in those of other cytokines or conventional markers, compared with those without chorioamnionitis. A positive correlation was observed between maternal and cord serum IL‐8 levels. Maternal IL‐8 showed the highest predictive value for diagnosis of histological chorioamnionitis. Conclusion: Measurement of maternal IL‐8 is useful for rapid prenatal screening of histological chorioamnionitis at term.

Endoscopic third ventriculostomy during pregnancy

ology (CVUE), was observed. The frequency of maternal complications in scleroderma patients is not increased compared with healthy controls, except for renal crisis [1]. Prematurity and preterm births are amajor problem. In a recent study, pretermbirths occurred in 29% of scleroderma pregnancies [3]. Detailed descriptions of placental findings in scleroderma are limited and include chronic villitis associated with decidual vasculopathy, placental infarcts, abruption, as well as normal placentas [2]. In a recent study of 13 placentas from 8 women with scleroderma, decidual vasculopathy was observed in 5 placentas and was associated with poor perinatal outcome [4]. Decidual vasculopathy reflects pathological deviations from normal placentation, such as fibrinoid necrosis of vessel walls, with or without foamy macrophages (atherosis), vasculitis, and presence of small muscularized thick-walled blood vessels [5]. In the present case PMD, and not decidual vasculopathy, was the most prominent placental finding. PMD is associated with IUGR. The typical features of PMD, that were also observed in this case, are stem villi with excessive proliferation of mesenchymatous tissue, with foci of myxoid degeneration, and large stromalmacrophages and vessels with fibromuscular sclerosis and thrombosis [6]. In conclusion, PMD, decidual vasculopathy, and other placental lesions associated with compromised uteroplacental perfusion may appear in scleroderma and are correlated with poor perinatal outcome.