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胎儿来源的髓样分化因子88信号传导导致妊娠期疟疾期间不良妊娠结局。

Fetal-Derived MyD88 Signaling Contributes to Poor Pregnancy Outcomes During Gestational Malaria.

作者信息

Barboza Renato, Hasenkamp Lutero, Barateiro André, Murillo Oscar, Peixoto Erika Paula Machado, Lima Flávia Afonso, Reis Aramys Silva, Gonçalves Lígia Antunes, Epiphanio Sabrina, Marinho Claudio R F

机构信息

Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, Brazil.

Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.

出版信息

Front Microbiol. 2019 Jan 29;10:68. doi: 10.3389/fmicb.2019.00068. eCollection 2019.

DOI:10.3389/fmicb.2019.00068
PMID:30761111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6362412/
Abstract

Placental malaria (PM) remains a severe public health problem in areas of high malaria transmission. Despite the efforts to prevent infection poor outcomes in endemic areas, there is still a considerable number of preterm births and newborns with low birth weight resulting from PM. Although local inflammation triggered in response to malaria is considered crucial in inducing placental damage, little is known about the differential influence of maternal and fetal immune responses to the disease progression. Therefore, using a PM mouse model, we sought to determine the contribution of maternal and fetal innate immune responses to PM development. For this, we conducted a series of cross-breeding experiments between mice that had differential expression of the MyD88 adaptor protein to obtain mother and correspondent fetuses with distinct genetic backgrounds. By evaluating fetal weight and placental vascular spaces, we have shown that the expression of MyD88 in fetal tissue has a significant impact on PM outcomes. Our results highlighted the existence of a distinct contribution of maternal and fetal immune responses to PM onset. Thus, contributing to the understanding of how inflammatory processes lead to the dysregulation of placental homeostasis ultimately impairing fetal development.

摘要

胎盘疟疾(PM)在疟疾高传播地区仍然是一个严重的公共卫生问题。尽管在疟疾流行地区人们努力预防感染并改善不良结局,但仍有相当数量的早产和低出生体重新生儿是由胎盘疟疾导致的。尽管因疟疾引发的局部炎症被认为在导致胎盘损伤方面至关重要,但关于母体和胎儿免疫反应对疾病进展的不同影响却知之甚少。因此,我们使用胎盘疟疾小鼠模型,试图确定母体和胎儿固有免疫反应对胎盘疟疾发展的作用。为此,我们在髓样分化因子88(MyD88)衔接蛋白表达不同的小鼠之间进行了一系列杂交实验,以获得具有不同遗传背景的母体和相应胎儿。通过评估胎儿体重和胎盘血管间隙,我们发现胎儿组织中MyD88的表达对胎盘疟疾的结局有显著影响。我们的结果突出表明母体和胎儿免疫反应对胎盘疟疾发病存在不同作用。因此,有助于理解炎症过程如何导致胎盘内环境稳态失调,最终损害胎儿发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/dbb9ab84d36a/fmicb-10-00068-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/5af5e6f45bdb/fmicb-10-00068-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/e0a078160c1d/fmicb-10-00068-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/194cdd7fff7f/fmicb-10-00068-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/dbb9ab84d36a/fmicb-10-00068-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/5af5e6f45bdb/fmicb-10-00068-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/e0a078160c1d/fmicb-10-00068-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/194cdd7fff7f/fmicb-10-00068-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee3/6362412/dbb9ab84d36a/fmicb-10-00068-g004.jpg

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本文引用的文献

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Burden, pathology, and costs of malaria in pregnancy: new developments for an old problem.妊娠疟疾的负担、病理和成本:老问题的新进展。
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