Congenital Chagas disease, caused by Trypanosoma cruzi (T. cruzi), is partially responsible for the increasing globalization of Chagas disease despite its low transmission. During congenital transmission, the parasite reaches the fetus by crossing the placental barrier. However, the success or impairment of congenital transmission of the parasite is the product of a complex interaction between the parasite, the maternal and fetus/newborn immune responses and placental factors. There is other evidence apart from the low congenital transmission rates, which suggests the presence of defense mechanisms against T. cruzi. Thus, the typical amastigote nests (intracellular parasites) cannot be observed in placentas from mothers with chronic Chagas disease nor in human placental chorionic villi explants infected in vitro with the parasite. In the latter, only a few parasite antigens and DNA are identified. Accordingly, other infections of the placenta are not commonly observed. All these evidences suggest that the placenta can mount defense mechanisms against T. cruzi.
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Cover Image
Cover Image
Trypanosoma brucei, the causative agent of African sleeping sickness. Among the parasitology topics covered in this issue are perspectives on various aspects of trypanosome biology: Kemmerling et al. (pages 573–577) look at the immune response against Trypanosoma cruzi in the human placenta, while Maya et al. (pages 579–584) discuss therapeutic strategies in chronic Chagas cardiomyopathy, which is caused by T. cruzi. In addition, McCulloch et al. (pages 585–592) and Ooi and Rudenko (pages 593–600) explore antigenic variation in trypanosomes. Image credit: Kateryna Kon (Shutterstock ID: 520410646).
The immune response against Trypanosoma cruzi in the human placenta
Roberto Docampo, Ulrike Kemmerling, Christian Castillo, Ana Liempi, Lisvaneth Medina, Ileana Carrillo, Daniel Droguett, Juan D. Maya, Norbel Galanti; The immune response against Trypanosoma cruzi in the human placenta. Emerg Top Life Sci 22 December 2017; 1 (6): 573–577. doi: https://doi.org/10.1042/ETLS20170115
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