CONGENITAL TRANSMISSION OF PROTOZOA: PLACENTAL INFECTION BY TRYPANOSOMA CRUZI

C. DÍAZ-LUJÁN ; M.F TRIQUELL ; E.M. BOLATTI; M.J MOREIRA ESPINOSA; D. HARDISSON; C. CASTILLO; U. KEMMERLING; R. E. FRETES

Mar del Plata

Congreso; VI SLIMP; 2015

Latin American Society for Maternal Fetal Interaction and Placenta

Chagas disease and its congenital transmission are caused by the protozoan Trypanosoma cruzi. The maternal-fetal transmission has spread the disease into non-endemic countries. Its incidence is low and the complete placental barrier limits the placental infection. Since discontinuities in the placental barrier have been described, the Objectives and Methods were to analyze the susceptibility of placental barrier cells to infection by T. cruzi and the role of nitric oxide by using monolayers of trophoblasts in vitro, placental explants in an in vitro-ex vivo experimental design and placentas from chagasic women. Results: The syncytiotrophoblast (STB) was significantly less infected than the cytotrophoblast (CTB), indicating that the inner cells of chorionic villi are more susceptible to infection than the cells which are in contact with the maternal blood, explaining at least in part the resistance of transmission to the fetus. Nitric oxide (NO) levels increased when STB was present and correlated significantly with decreased viability of parasite cells in the culture media (r¼0.93). Moreover, expression of endothelial Nitric Oxide Synthase (eNOS) by STB, one of the isoenzymes that produces NO, decreased significantly in placentas with maternal-fetal transmission of Chagas, which were also positive to T. cruzi DNA by PCR technique, indicating that this gas plays an important role in the clearance of parasites in the placental environment, in placental infection and/or congenital transmission. Conclusion: These results support that STB plays a key role limiting the infection of chorionic villi by T. cruzi, via clearing parasites out of the placental environment and via NO producing enzymes. Thus, these results establish that there was a placental environment deleterious to T. cruzi and that discontinuities in the placental barrier and/or deficiencies in placental defenses, such as eNOS, facilitate the infection of placental tissue and maternal-fetal transmission of Chagas