Impact of chorioamnionitis on maternal and fetal levels of proinflammatory S100A12.

Histologic chorioamnionitis (HCA) may lead to the fetal inflammatory response syndrome (FIRS). The aim of this pilot study was to evaluate S100A12, a marker of innate immune activation, in mothers with or without HCA and in their infants. Concentrations of S100A12, interleukin 6 (IL-6), and C-reactive protein (CRP) were evaluated in maternal, cord, and neonatal blood of very preterm infants. Histologic examinations of the placenta and umbilical cords were performed. The 48 mother-neonate pairs enrolled were subdivided into two groups: HCA group (N = 15) and control group without HCA (N = 33). Maternal S100A12 levels were similar between HCA and control group. Similarly, S100A12 concentrations in cord and neonatal blood did not differ between the groups. However, high S100A12 concentrations were detected in cord and neonatal blood of two out of three neonates exposed to HCA associated with advanced funisitis. Concentrations of IL-6 and CRP were higher in maternal blood of the HCA group compared with controls (p < 0.05, p < 0.001; respectively), but no differences in cord or neonatal blood was found.Conclusion:S100A12 did neither identify mothers with HCA nor very preterm infants exposed to HCA. It is currently unknown if S100A12 may identify neonates with FIRS. What is known: • Histologic chorioamnionitis (HCA) may lead to the fetal inflammatory response syndrome (FIRS). • S100A12 represents an early, sensitive, and specific diagnostic marker of inflammatory processes. What is new: • S100A12 did neither identify mothers with HCA nor very preterm infants exposed to HCA. • It is currently still unclear if S100A12 has a potential in identifying preterm infants with FIRS.

Interleukin-22: biomarker of maternal and fetal inflammation?

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.