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Am J Reprod Immunol. 2018 Jul;80(1):e12852. doi: 10.1111/aji.12852. Epub 2018 Mar 25.

Nitric oxide synthase and oxidative-nitrosative stress play a key role in placental infection by Trypanosoma cruzi.

Author information

1
Biología Celular, Histología y Embriología, Fac. Cs. Médicas, Universidad Nacional de Córdoba-INICSA (CONICET), Córdoba, Argentina.
2
Histología y Citología, Instituto de Ciencias Humanas, Universidad Nacional de Villa María, Córdoba, Argentina.
3
Departamento de Anatomía-Facultad de Agronomía y Veterinaria, Universidad Nacional Río Cuarto, Córdoba, Argentina.
4
Laboratorio de Biología Molecular de la Enfermedad de Chagas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Hector Torres" (INGEBI-CONICET), Buenos Aires, Argentina.
5
Cátedra de Física Biomédica, Facultad Cs. Médicas, Universidad Nacional Córdoba, Córdoba-INICSA (CONICET), Córdoba, Argentina.
6
IICSHUM-Histología y Embriología, Universidad Nacional de La Rioja, La Rioja, Argentina.

Abstract

PROBLEM:

The innate immune response of the placenta may participate in the congenital transmission of Chagas disease through releasing reactive oxygen and nitrogen intermediates.

METHOD OF STUDY:

Placental explants were cultured with 1 × 106 and 1 × 105 trypomastigotes of Tulahuen and Lucky strains and controls without parasites, and with the addition of nitric oxide synthase inhibitor Nω-Nitro-l-arginine methyl ester (l-NAME) and N-acetyl cysteine (NAC) as the reactive oxygen species (ROS) scavenger. Detachment of the syncytiotrophoblast (STB) was examined by histological analysis, and the nitric oxide synthase, endothelial (eNOS), and nitrotyrosine expressions were analyzed by immunohistochemistry, as well as the human chorionic gonadotrophin (hCG) levels in the culture supernatant through ELISA assays. Parasite load with qPCR using Taqman primers was quantified.

RESULTS:

The higher number of T. cruzi (106 ) increased placental infection, eNOS expression, nitrosative stress, and STB detachment, with the placental barrier being injured by oxidative stress.

CONCLUSION:

The higher number of parasites caused deleterious consequences to the placental barrier, and the inhibitors (l-NAME and NAC) prevented the damage caused by trypomastigotes in placental villi but not that of the infection. Moreover, trophoblast eNOS played a key role in placental infection with the highest inoculum of Lucky, demonstrating the importance of the enzyme and nitrosative-oxidative stress in Chagas congenital transmission.

KEYWORDS:

Trypanosoma cruzi ; congenital chagas transmission; nitric oxide synthase; oxidative stress; placenta; trophoblast

PMID:
29577492
DOI:
10.1111/aji.12852

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