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

Bibliographic Details
Title: Fetal-Derived MyD88 Signaling Contributes to Poor Pregnancy Outcomes During Gestational Malaria
Authors: Renato Barboza, Lutero Hasenkamp, André Barateiro, Oscar Murillo, Erika Paula Machado Peixoto, Flávia Afonso Lima, Aramys Silva Reis, Lígia Antunes Gonçalves, Sabrina Epiphanio, Claudio R. F. Marinho
Source: Frontiers in Microbiology, Vol 10 (2019)
Publisher Information: Frontiers Media S.A., 2019.
Publication Year: 2019
Collection: LCC:Microbiology
Subject Terms: mouse model, pregnancy, placenta, malaria, MyD88, Plasmodium berghei, Microbiology, QR1-502
More Details: Placental malaria (PM) remains a severe public health problem in areas of high malaria transmission. Despite the efforts to prevent infection poor outcomes in Plasmodium 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1664-302X
Relation: https://www.frontiersin.org/article/10.3389/fmicb.2019.00068/full; https://doaj.org/toc/1664-302X
DOI: 10.3389/fmicb.2019.00068
Access URL: https://doaj.org/article/c80d6d4923c9412fbfb45e4bce269d4e
Accession Number: edsdoj.80d6d4923c9412fbfb45e4bce269d4e
Database: Directory of Open Access Journals
More Details
ISSN:1664302X
DOI:10.3389/fmicb.2019.00068
Published in:Frontiers in Microbiology
Language:English