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Hepcidin, an Iron Regulatory Hormone of Innate Immunity, is Differentially Expressed in Premature Fetuses with Early-Onset Neonatal Sepsis
Journal article   Open access   Peer reviewed

Hepcidin, an Iron Regulatory Hormone of Innate Immunity, is Differentially Expressed in Premature Fetuses with Early-Onset Neonatal Sepsis

Sammy M. Tabbah, Catalin S. Buhimschi, Katherine Rodewald-Millen, Christopher R. Pierson, Vineet Bhandari, Philip Samuels and Irina A. Buhimschi
American journal of perinatology, v 35(9), pp 865-872
Jul 2018
PMID: 29532452
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412256View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Original Article
Abstract Objective  Hepcidin, a mediator of innate immunity, binds the iron exporter ferroportin, leading to functional hypoferremia through intracellular iron sequestration. We explored hepcidin–ferroportin interactions in neonates clinically diagnosed with early-onset neonatal sepsis (EONS). Study Design  Hepcidin and interleukin (IL)-6 were quantified by enzyme-linked immunosorbent assay (ELISA) in 92 paired cord blood–maternal blood samples in the following groups: “Yes” EONS ( n  = 41, gestational age [GA] 29 ± 1 weeks) and “No” EONS ( n  = 51, GA 26 ± 1 weeks). Placental hepcidin and ferroportin expression were evaluated by immunohistochemistry and real-time-polymerase chain reaction (RT-PCR). Liver hepcidin and ferroportin expression patterns were ascertained in autopsy specimens of neonates ( n  = 8) who died secondary to culture-proven sepsis. Results  Cord blood hepcidin was significantly elevated (GA corrected, p  = 0.018) and was positively correlated with IL-6 ( r  = 0.379, p  = 0.001) in EONS. Hepcidin localized at syncytiotrophoblast and fetal vascular endothelium. Placental ferroportin, but not hepcidin mRNA correlated with cord blood hepcidin levels ( r  = 0.46, p  = 0.039) and funisitis severity ( r  = 0.50, p  = 0.018). Newborns who died from sepsis ( n  = 4) had higher hepatic hepcidin and iron sequestration, but lower ferroportin staining than those who died of nonsepsis causes ( n  = 4). Conclusion  Premature fetuses with EONS have elevated circulating hepcidin, likely related to lower placenta and liver ferroportin expression. Fetal hepcidin–ferroportin interaction appears to play a role in EONS pathophysiology independent of maternal response to intrauterine inflammation.

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Collaboration types
Domestic collaboration
Web of Science research areas
Obstetrics & Gynecology
Pediatrics
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