Abstract

Introduction: The congenital transmission of Trypanosoma cruzi (T. cnizi) is responsible for one-third of new Chagas disease cases each year. During congenital transmission, the parasite breaks down the placental barrier formed by the trophoblast, basal laminae and villous stroma. The observation that only 5% of infected mothers transmit the parasite to the fetus implies that the placenta may impair parasite transmission. The trophoblast undergoes continuous epithelial turnover, which is considered part of innate immunity. Therefore, we propose that T. cruzi induces differentiation in the trophoblast as part of a local antiparasitic mechanism of the placenta. Methods: We analyzed beta-human chorionic gonadotropin (beta-hCG) and syncytin protein expression in HPCVE and BeWo cells using immunofluorescence and western blotting. Additionally, beta-hCG secretion into the culture medium was measured by ELISA. We assessed the differentiation of trophoblastic cells in BeWo cells using the two-color fusion assay and by determining desmoplakin re-distribution. Results: T. cnizi trypomastigotes induce beta-hCG secretion and protein expression as well as syncyntin protein expression in HPCVE and BeWo cells. Addionally, the parasite induces the trophoblast fusion of BeWo cells. Discussion: T cruzi induces differentiation of the trophoblast, which may contribute to increase the trophoblast turnover. The turnover could be a component of local antiparasitic mechanisms in the human placenta. (C) 2014 Elsevier Ltd. All rights reserved.