Kemmerling Ulrike, Castillo Christian, Liempi Ana, Medina Lisvaneth, Carrillo Ileana, Droguett Daniel, Maya Juan D, Galanti Norbel
Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Independencia 1027, Santiago, Chile.
Emerg Top Life Sci. 2017 Dec 22;1(6):573-577. doi: 10.1042/ETLS20170115.
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.
先天性恰加斯病由克氏锥虫（T. cruzi）引起，尽管其传播率较低，但它在一定程度上导致了恰加斯病全球化的加剧。在先天性传播过程中，寄生虫通过胎盘屏障到达胎儿体内。然而，寄生虫先天性传播的成功或受阻是寄生虫、母体以及胎儿/新生儿免疫反应和胎盘因素之间复杂相互作用的结果。除了先天性传播率较低之外，还有其他证据表明存在针对克氏锥虫的防御机制。因此，在患有慢性恰加斯病的母亲的胎盘中，以及在体外感染该寄生虫的人胎盘绒毛膜绒毛外植体中，均无法观察到典型的无鞭毛体巢（细胞内寄生虫）。在后一种情况下，仅能鉴定出少数寄生虫抗原和DNA。相应地，胎盘的其他感染也并不常见。所有这些证据表明，胎盘能够对克氏锥虫产生防御机制。
