Maternal Trypanosoma cruzi-Specific Antibodies and Worsening of Acute Infection in Mouse Offspring

Araujo, Sonia; Rivera, M. T.; Bouhdidi, A el; Maertelaer, Viviane De; Carlier, Yves

doi:10.4269/ajtmh.1996.54.13

Cited by 7 publications

(3 citation statements)

References 2 publications

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“…It was verified that injected Ab were transferred to offspring. When infected two months after birth (as in the experiments mentioned above), offspring of mice treated with chronic serum or purified Ab displayed significantly higher parasitemia and mortality rates than offspring from mothers receiving control serum or immunoglobulins unrelated to T. cruzi (30). These results indicate an ADE-like phenomenon in experimental T. cruzi infection, and particularly in mice receiving maternally derived Ab.…”

Section: Experimental Evidences Of Ade Of T Cruzi Infection In Mouse Pups Displaying Maternally Transferred Abmentioning

confidence: 75%

“…Our report performed with uninfected mice having received purified T. cruzi-specific Ab during gestation and lactation period, showed that Ab levels were reduced by 4 times in offspring at the weaning time (i.e. 3 weeks after birth), compared to the maternal Ab level (30). Other infection models indicate that such transferred Ab can persist more than 6 weeks after birth, i.e.…”

Section: Vertical Transmission Of T Cruzi-specific Abmentioning

confidence: 83%

“…In murine infection with T. cruzi, maternal-offspring transfer of Ab occurs through lactation (28)(29)(30), but direct kinetic studies of such transfer are lacking. Our report performed with uninfected mice having received purified T. cruzi-specific Ab during gestation and lactation period, showed that Ab levels were reduced by 4 times in offspring at the weaning time (i.e.…”

Section: Vertical Transmission Of T Cruzi-specific Abmentioning

confidence: 99%

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

2021

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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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Section: Experimental Evidences Of Ade Of T Cruzi Infection In Mouse Pups Displaying Maternally Transferred Abmentioning

confidence: 75%

Section: Vertical Transmission Of T Cruzi-specific Abmentioning

confidence: 83%

Section: Vertical Transmission Of T Cruzi-specific Abmentioning

confidence: 99%

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

2021

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Pregnancy and Susceptibility to Parasites

Henriquez¹,

Menzies²,

Roberts

2009

Sex Hormones and Immunity to Infection

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Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

2015

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The aim of this paper is to discuss the main ecological interactions between the parasite Trypanosoma cruzi and its hosts, the mother and the fetus, leading to the transmission and development of congenital Chagas disease. One or several infecting strains of T. cruzi (with specific features) interact with: (i) the immune system of a pregnant woman whom responses depend on genetic and environmental factors, (ii) the placenta harboring its own defenses, and, finally, (iii) the fetal immune system displaying responses also susceptible to be modulated by maternal and environmental factors, as well as his own genetic background which is different from her mother. The severity of congenital Chagas disease depends on the magnitude of such final responses. The paper is mainly based on human data, but integrates also complementary observations obtained in experimental infections. It also focuses on important gaps in our knowledge of this congenital infection, such as the role of parasite diversity vs host genetic factors, as well as that of the maternal and placental microbiomes and the microbiome acquisition by infant in the control of infection. Investigations on these topics are needed in order to improve the programs aiming to diagnose, manage and control congenital Chagas disease.

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Maternal Trypanosoma cruzi-Specific Antibodies and Worsening of Acute Infection in Mouse Offspring

Cited by 7 publications

References 2 publications

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

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

Pregnancy and Susceptibility to Parasites

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

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