Key result
T. cruzi infection in placentas from asymptomatic mothers induces destruction of the syncytiotrophoblast and villous stroma, and disorganization of the basal lamina and collagen I.
Observational
T. cruzi infection induces reorganization of the placental extracellular matrix, which may play a role in regulating host immune responses and congenital transmission.
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May inform congenital Chagas transmission risk assessment; leaves open mechanistic and predictive validation in larger cohorts.
Chagas disease, produced by the protozoan Trypanosoma cruzi (T. cruzi), is one of the most frequent endemic diseases in Latin America. In spite the fact that in the past few years T. cruzi congenital transmission has become of epidemiological importance, studies about this mechanism of infection are scarce. In order to explore some morphological aspects of this infection in the placenta, we analyzed placentas from T. cruzi-infected mothers by immunohistochemical and histochemical methods. Infection in mothers, newborns, and placentas was confirmed by PCR and by immunofluorescence in the placenta. T. cruzi-infected placentas present destruction of the syncytiotrophoblast and villous stroma, selective disorganization of the basal lamina, and disorganization of collagen I in villous stroma. Our results suggest that the parasite induces reorganization of this tissue component and in this way may regulate both inflammatory and immune responses in the host. Changes in the ECM of placental tissues, together with the immunological status of mother and fetus, and parasite load may determine the probability of congenital transmission of T. cruzi.
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Duaso et al. (2011) conducted an observational in Asymptomatic Chagas Disease. T. cruzi infection was evaluated on Morphological changes in the placenta (extracellular matrix reorganization). T. cruzi infection in placentas from asymptomatic mothers induces destruction of the syncytiotrophoblast and villous stroma, and disorganization of the basal lamina and collagen I.
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