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Updated: Feb 13, 2026

Human Placental and Decidual Organ Cultures to Study Infections at the Maternal-fetal Interface
Published on: July 21, 2016
Maternal serum levels and placental expression of hepcidin in preeclampsia
Simona Cardaropoli1, Tullia Todros1, Anna Maria Nuzzo2
1Department of Surgical Sciences, University of Turin, Via Ventimiglia 3, 10126 Turin, Italy; Department of Obstetrics and Neonatology, Sant'Anna Hospital, Corso Spezia 60, 10126 Turin, Italy.
Insights
Hepcidin, an iron regulator, may signal infection in preeclampsia (PE). While placental hepcidin was lower in PE, higher early pregnancy serum hepcidin levels may predict PE development.
Area of Science:
- Reproductive biology
- Immunology
- Iron metabolism
Background:
- Preeclampsia (PE) is a complex pregnancy disorder potentially linked to infection.
- Hepcidin, an antimicrobial peptide regulating iron, is influenced by inflammation and infection.
Purpose of the Study:
- To investigate hepcidin's role as a potential marker for infection in preeclampsia.
- To assess maternal serum and placental hepcidin levels in preeclampsia and normal pregnancies.
Main Methods:
- Cross-sectional and prospective studies were conducted.
- Maternal serum and placental hepcidin levels were measured using ELISA and Real-Time PCR.
- Early pregnancy serum hepcidin was assessed in women who later developed PE versus controls.
Main Results:
- Placental hepcidin expression (protein and gene) was decreased in PE placentae.
- Maternal serum hepcidin showed no significant difference in PE versus controls at the time of diagnosis.
- Elevated maternal serum hepcidin in early pregnancy predicted subsequent PE development.
Conclusions:
- Altered placental hepcidin expression in PE may indicate local inflammatory or infective processes.
- Increased maternal serum hepcidin in early pregnancy could serve as an early predictive marker for preeclampsia.
- Hepcidin's role highlights the importance of the inflammatory status preceding PE onset.
Abstract:
Preeclampsia (PE) is a multifactorial pregnancy-induced syndrome and infection could have a role in its etiopathogenesis. Hepcidin, central regulator of iron homeostasis, is an antimicrobial peptide induced by inflammatory/infective stimuli. Therefore, hepcidin could be a good nonspecific marker of infection in PE. In a cross-sectional study, we assessed maternal serum levels (ELISA) and placental expression (Real-Time PCR and ELISA) of hepcidin in PE and normal pregnancies. In a prospective study, hepcidin maternal serum levels were assessed in early pregnancy before PE onset and in age matched controls. Hepcidin protein and gene expressions were significantly decreased in PE placentae with normal fetal growth compared to controls and PE with Fetal Growth Restriction (FGR), respectively. In contrast, we did not find significant differences in maternal serum hepcidin levels in PE vs gestational age-matched controls. Hepcidin serum levels in the first half of pregnancy were found significantly higher in women who subsequently developed PE compared to mothers having a physiological pregnancy until term. Altered hepcidin expression in PE placentae could be explained by direct infective/inflammatory stimuli. Furthermore, high hepcidin levels in maternal serum could be an early marker of PE, further emphasizing the role of inflammatory status before symptoms onset in PE.
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