TY - JOUR
T1 - Interleukin-22: Biomarker of maternal and fetal inflammation?
AU - Bersani, Iliana
AU - De Carolis, Maria Pia
AU - Rossi, Esther
AU - De Carolis, Sara
AU - Rubortone, Serena Antonia
AU - Romagnoli, Costantino
PY - 2015
Y1 - 2015
N2 - 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
AB - 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
KW - inflammation
KW - interleukin 22
KW - inflammation
KW - interleukin 22
UR - http://hdl.handle.net/10807/62976
U2 - 10.1007/s12026-014-8568-2
DO - 10.1007/s12026-014-8568-2
M3 - Article
SN - 0257-277X
VL - 61
SP - 4
EP - 10
JO - Immunologic Research
JF - Immunologic Research
ER -