Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?

The newborns of women infected with the parasite Trypanosoma cruzi (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route). Congenital Chagas disease can induce high levels of neonatal morbidity and mortality. Parasite-infected preg...

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Main Authors: Yves Carlier, Carine Truyens, Eric Muraille
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-09-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2021.723516/full
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author Yves Carlier
Yves Carlier
Carine Truyens
Eric Muraille
author_facet Yves Carlier
Yves Carlier
Carine Truyens
Eric Muraille
author_sort Yves Carlier
collection DOAJ
description The newborns of women infected with the parasite Trypanosoma cruzi (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route). Congenital Chagas disease can induce high levels of neonatal morbidity and mortality. Parasite-infected pregnant women transmit antibodies to their fetus. Antibodies, by opsonizing parasites, can promote phagocytosis and killing of T. cruzi by cells expressing FcγR, on the mandatory condition that such cells are sufficiently activated in an inflammatory context. Antibody-dependent enhancement (ADE) is a mechanism well described in viral infections, by which antibodies enhance entry of infectious agents into host cells by exploiting the phagocytic FcγR pathway. Previously reported Chagas disease studies highlighted a severe reduction of the maternal-fetal/neonatal inflammatory context in parasite-transmitting pregnant women and their congenitally infected newborns. Otherwise, experimental observations brought to light ADE of T. cruzi infection (involving FcγR) in mouse pups displaying maternally transferred antibodies, out of an inflammatory context. Herein, based on such data, we discuss the previously unconsidered possibility of a role of ADE in the trans-placental parasite transmission, and/or the development of severe and mortal clinical forms of congenital/neonatal Chagas disease in newborns of T. cruzi-infected mothers.
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spelling doaj.art-6c3c54da7fec4fe88424b6a94662521c2022-12-21T23:32:23ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-09-011210.3389/fimmu.2021.723516723516Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?Yves Carlier0Yves Carlier1Carine Truyens2Eric Muraille3Laboratoire de Parasitologie, Faculté de Médecine, Université Libre de Bruxelles (ULB), Bruxelles, BelgiumDepartment of Tropical Medicine, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, United StatesLaboratoire de Parasitologie, Faculté de Médecine, Université Libre de Bruxelles (ULB), Bruxelles, BelgiumLaboratoire de Parasitologie, Faculté de Médecine, Université Libre de Bruxelles (ULB), Bruxelles, BelgiumThe newborns of women infected with the parasite Trypanosoma cruzi (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route). Congenital Chagas disease can induce high levels of neonatal morbidity and mortality. Parasite-infected pregnant women transmit antibodies to their fetus. Antibodies, by opsonizing parasites, can promote phagocytosis and killing of T. cruzi by cells expressing FcγR, on the mandatory condition that such cells are sufficiently activated in an inflammatory context. Antibody-dependent enhancement (ADE) is a mechanism well described in viral infections, by which antibodies enhance entry of infectious agents into host cells by exploiting the phagocytic FcγR pathway. Previously reported Chagas disease studies highlighted a severe reduction of the maternal-fetal/neonatal inflammatory context in parasite-transmitting pregnant women and their congenitally infected newborns. Otherwise, experimental observations brought to light ADE of T. cruzi infection (involving FcγR) in mouse pups displaying maternally transferred antibodies, out of an inflammatory context. Herein, based on such data, we discuss the previously unconsidered possibility of a role of ADE in the trans-placental parasite transmission, and/or the development of severe and mortal clinical forms of congenital/neonatal Chagas disease in newborns of T. cruzi-infected mothers.https://www.frontiersin.org/articles/10.3389/fimmu.2021.723516/fullTrypanosoma cruzichagas diseasecongenital/neonatal infectionantibodiesFcRantibody-dependent enhancement
spellingShingle Yves Carlier
Yves Carlier
Carine Truyens
Eric Muraille
Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
Frontiers in Immunology
Trypanosoma cruzi
chagas disease
congenital/neonatal infection
antibodies
FcR
antibody-dependent enhancement
title Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
title_full Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
title_fullStr Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
title_full_unstemmed Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
title_short Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?
title_sort is antibody dependent enhancement of trypanosoma cruzi infection contributing to congenital neonatal chagas disease
topic Trypanosoma cruzi
chagas disease
congenital/neonatal infection
antibodies
FcR
antibody-dependent enhancement
url https://www.frontiersin.org/articles/10.3389/fimmu.2021.723516/full
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