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Updated: Apr 20, 2026

Isolation of Leukocytes from the Human Maternal-fetal Interface
Published on: May 21, 2015
Interleukin-22: biomarker of maternal and fetal inflammation?
Iliana Bersani1, Maria Pia De Carolis, Dirk Foell
1Department of Medical and Surgical Neonatology, Bambino Gesù Children's Hospital, Rome, Italy.
Histologic chorioamnionitis (HCA) is an intrauterine status of inflammation which may lead to the fetal inflammatory response syndrome. Inflammation is a pathogenetic mechanism also of preeclampsia, although not of microbial origin. The aim of the present pilot study was to evaluate the pattern of inflammatory cytokines in mothers and high-risk preterm infants during the perinatal period. Concentrations of proinflammatory and anti-inflammatory cytokines and C-reactive protein were evaluated in maternal, cord, and neonatal blood of very preterm infants <1,500 g birth weight. Histologic examinations of placentae and umbilical cords were performed. The 65 mother-neonate pairs enrolled were subdivided into three groups: (1) HCA group (n = 15), (2) preeclampsia group (n = 17), and (3) control group, in the absence of HCA/preeclampsia (n = 33). Maternal Interleukin (IL)-6 levels were significantly higher in women of the HCA group compared with the preeclampsia and control groups (p < 0.05). IL-22 was detected in nearly all maternal samples [median value 693.115 pg/ml (599.91-809.91 pg/ml)], with no statistical difference between the groups, but with a tendency to increased levels among preeclamptic women. Increased concentrations of IL-22 were detected in cord blood of neonates exposed to preeclampsia, compared with controls and infants exposed to HCA (p < 0.05). We speculate that the tendentially higher concentrations of IL-22 in preeclamptic mothers and the significantly higher concentrations in cord blood may reflect placental dysfunction and the underlying reparative processes at the maternal-fetal interface. Therefore, IL-22 could be an important biomarker of inflammation in preeclampsia.
Histologic chorioamnionitis (HCA) is an intrauterine status of inflammation which may lead to the fetal inflammatory response syndrome. Inflammation is a pathogenetic mechanism also of preeclampsia, although not of microbial origin. The aim of the present pilot study was to evaluate the pattern of inflammatory cytokines in mothers and high-risk preterm infants during the perinatal period. Concentrations of proinflammatory and anti-inflammatory cytokines and C-reactive protein were evaluated in maternal, cord, and neonatal blood of very preterm infants <1,500 g birth weight. Histologic examinations of placentae and umbilical cords were performed. The 65 mother-neonate pairs enrolled were subdivided into three groups: (1) HCA group (n = 15), (2) preeclampsia group (n = 17), and (3) control group, in the absence of HCA/preeclampsia (n = 33). Maternal Interleukin (IL)-6 levels were significantly higher in women of the HCA group compared with the preeclampsia and control groups (p < 0.05). IL-22 was detected in nearly all maternal samples [median value 693.115 pg/ml (599.91-809.91 pg/ml)], with no statistical difference between the groups, but with a tendency to increased levels among preeclamptic women. Increased concentrations of IL-22 were detected in cord blood of neonates exposed to preeclampsia, compared with controls and infants exposed to HCA (p < 0.05). We speculate that the tendentially higher concentrations of IL-22 in preeclamptic mothers and the significantly higher concentrations in cord blood may reflect placental dysfunction and the underlying reparative processes at the maternal-fetal interface. Therefore, IL-22 could be an important biomarker of inflammation in preeclampsia.
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