Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.7/369
Título: Iron overload in Plasmodium berghei-infected placenta as a pathogenesis mechanism of fetal death
Autor: Penha-Gonçalves, Carlos
Gozzelino, Raffaella
de Moraes, Luciana V.
Palavras-chave: pregnancy malaria
fetal death
Data: 1-Jul-2014
Editora: Frontiers Research Foundation
Citação: Penha-Gonçalves C, Gozzelino R and de Moraes LV (2014) Iron overload in Plasmodium berghei-infected placenta as a pathogenesis mechanism of fetal death. Front. Pharmacol. 5:155. doi: 10.3389/fphar.2014.00155
Resumo: Plasmodium infection during gestation may lead to severe clinical manifestations including abortion, stillbirth, intrauterine growth retardation, and low birth weight. Mechanisms underlying such poor pregnancy outcomes are still unclear. In the animal model of severe placental malaria (PM), in utero fetal death frequently occurs and mothers often succumb to infection before or immediately after delivery. Plasmodium berghei-infected erythrocytes (IEs) continuously accumulate in the placenta, where they are then phagocytosed by fetal-derived placental cells, namely trophoblasts. Inside the phagosomes, disruption of IEs leads to the release of non-hemoglobin bound heme, which is subsequently catabolized by heme oxygenase-1 into carbon monoxide, biliverdin, and labile iron. Fine-tuned regulatory mechanisms operate to maintain iron homeostasis, preventing the deleterious effect of iron-induced oxidative stress. Our preliminary results demonstrate that iron overload in trophoblasts of P. berghei-infected placenta is associated with fetal death. Placentas which supported normally developing embryos showed no iron accumulation within the trophoblasts. Placentas from dead fetuses showed massive iron accumulation, which was associated with parasitic burden. Here we present preliminary data suggesting that disruption of iron homeostasis in trophoblasts during the course of PM is a consequence of heme accumulation after intense IE engulfment. We propose that iron overload in placenta is a pathogenic component of PM, contributing to fetal death. The mechanism through which it operates still needs to be elucidated.
Descrição: This deposit is composed by the main article, and it hasn't any supplementary materials associated.
Peer review: yes
URI: http://hdl.handle.net/10400.7/369
DOI: 10.3389/fphar.2014.00155
Versão do Editor: http://journal.frontiersin.org/article/10.3389/fphar.2014.00155/abstract
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