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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Plasmodium falciparum infection dysregulates placental autophagy

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Author(s):
Lima, Flavia Afonso [1] ; Barateiro, Andre [1] ; Dombrowski, Jamille Gregorio [1] ; de Souza, Rodrigo Medeiros [2] ; Costa, Douglas de Sousa [1] ; Murillo, Oscar [1] ; Epiphanio, Sabrina [3] ; Goncalves, Ligia Antunes [1] ; Farias Marinho, Claudio Romero [1]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Parasitol, Sao Paulo - Brazil
[2] Univ Fed Acre, Multidisciplinary Ctr, Acre - Brazil
[3] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin & Toxicol Anal, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: PLoS One; v. 14, n. 12 DEC 5 2019.
Web of Science Citations: 0
Abstract

Plasmodium (P.) falciparum malaria during pregnancy has been frequently associated with severe consequences such as maternal anemia, abortion, premature birth, and reduced birth weight. Placental damage promotes disruption of the local homeostasis; though, the mechanisms underlying these events are still to be elucidated. Autophagy is a fundamental homeostatic mechanism in the natural course of pregnancy by which cells self-recycle in order to survive in stressful environments. Placentas from non-infected and P. falciparum-infected women during pregnancy were selected from a previous prospective cohort study conducted in the Brazilian Amazon (Acre, Brazil). Newborns from infected women experienced reduced birth weight (P = 0.0098) and placental immunopathology markers such as monocyte infiltrate (P < 0.0001) and IL-10 production (P = 0.0122). The placentas were evaluated for autophagy-related molecules. As a result, we observed reduced mRNA levels of ULK1 (P = 0.0255), BECN1 (P = 0.0019), and MAP1LC3B (P = 0.0086) genes in placentas from P. falciparum-infected, which was more striking in those diagnosed with placental malaria. Despite the protein levels of these genes followed the same pattern, the observed reduction was not statistically significant in placentas from P. falciparum-infected women. Nevertheless, our data suggest that chronic placental immunopathology due to P. falciparum infection leads to autophagy dysregulation, which might impair local homeostasis during malaria in pregnancy that may result in poor pregnancy outcomes. (AU)

FAPESP's process: 17/03939-7 - Impact of autophagy and inflammasome on the pathogenesis of Placental Malaria
Grantee:André Filipe Rivais Martins Barateiro
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 17/05782-8 - The study of vascular permeability in the malaria-associated acute respiratory distress syndrome
Grantee:Sabrina Epiphanio
Support Opportunities: Regular Research Grants
FAPESP's process: 13/16417-8 - Autophagy in placental malaria: effects and mechanisms
Grantee:Flávia Afonso Lima
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 12/04755-3 - Association of gestational malaria with intrauterine growth restriction and low birth weight in the far-western Brazilian Amazon
Grantee:Jamille Gregório Dombrowski
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 16/07030-0 - Characterization of autophagic activity and inflammasome in placental malaria
Grantee:Cláudio Romero Farias Marinho
Support Opportunities: Regular Research Grants
FAPESP's process: 15/06106-0 - The role of inflammasomes in the pathogenesis of malaria during pregnancy: effects and mechanisms
Grantee:Cláudio Romero Farias Marinho
Support Opportunities: Research Grants - Visiting Researcher Grant - International
FAPESP's process: 13/00981-1 - Characterization of the role of dendritic cells in the recrudescence of malaria in pregnancy
Grantee:Oscar Javier Murillo Gómez
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 18/20468-0 - Recrudescence of the malaria during pregnancy: effects and mechanisms
Grantee:Cláudio Romero Farias Marinho
Support Opportunities: Regular Research Grants