Human placental chorionic villi suffer oxidative stress produced by Trypanosoma cruzi.

MF TRIQUELL, CM DÍAZ- LUJÁN, MC ROMANINI, GM MAZZUDULLI, RE FRETES.

PLACENTA

W B SAUNDERS CO LTD

Lugar: Estados Unidos; Año: 2008 vol. 29 p. 133 - 133

0143-4004

Human placenta may act as a barrier to Trypanosoma cruzi, the causal agent of Chagas disease. Objectives: a) To analyse T. cruzi infection and alteration of chorionic villi structure in placental explants in vitro. b) To correlate Nitric Oxide (NO) production, endothelial Nitric Oxide Synthase (NOSe) expression and nitrosylation rate with infection and parasitic viability. Methods: Placental villi explants co-cultured for 24 h with 1x106 trypomastigotes of Tulahuen and Lucky strains (isolated from a congenital case). Histological and immunohistochemical analysis: of NOSe and Nitrotyrosine (NT) (Sigma- Scan); measurement of amastigotes per nest, infection area, detachment of syncytiotrophoblast, (Axiovision). In culture media: quantification of NO, hCG and live parasites. Results: Both strains had a similar area of infection and amastigotes per nest (p>0.05). Percentage of live parasites in co-culture supernatants was significantly higher with the congenital strain 11% than with Tulahuen 0.54%. Explants co-cultured with the Lucky strain showed higher detachment of STB (5.85%), smaller CTB proliferation (0.02%) and hCG levels than controls; Tulahuen co-cultures showed higher detachment of STB (18.9%) and CTB proliferation (0.88%) and decreased levels of hCG than controls. Nitrites concentration did not show significant differences p>0.05, but NOSe and NT positive areas were higher than controls (NOSe 19.99% Cont; 63.33% Tul) (NT, 0.51% Cont; 49.88% Lucky; 58.37% Tul). Conclusion: The infected chorionic villi present an increment in oxidative stress, probably associated with a rise in NO. These changes could be involved in the detachment of STB and participate in congenital infection. Supported by Secyt UNC UNLaR. P113 GRANULATED METRIAL GLAND CELLS IN A MOUSE MODEL OF BOVINE TRITRICHOMONOSIS M Woudwyka, C Monteavarob, C Cacciatob, P Sotob and C Barbeitoa. aFacultad de Ciencias Veterinarias, UNLP, La Plata, Argentina, bFacultad de Ciencias Veterinarias UNCPBA, Tandil, Argentina, marianawoudwyk02@hotmail.com The bovine tritrichomonosis is a venereal disease caused by to the protozoan Tritrichomonas foetus that produces embryonic death and abortion. The granulated metrial gland cells (GMG) present granules with cytotoxic molecules, positive to PAS and DBA lectin. From the 7th day of mouse gestation the GMG begin to increase its number in the decidua and in the 15th day they diminish to increase again near parturition. These cells regulate death in the uterine epithelium to allow the implantation; prevent the excessive growth of the trophoblast; support decidual health and favor the mother-foetal separation. Animals that lack these cells present abnormalities in the implantation sites. GMG?s lysis in the pregnant uteri infected with certain microorganisms is associated with loss of pregnancy. The aim of this work was to analyze changes in the GMG of the uterine horns in mice infected with T. foetus, to relate these cells and the embryonic early death in the tritrichomonosis. Samples of uteri from Balb/c mice with 5 to 10 days of pregnancy, infected by intravaginal via 10 days before the service. The samples were embebbed in paraffin and cuts were performed to apply the histochemistry tecnique of PAS. In the infected females GMG were small and diminished their numbers drastically. They presented scarce granules and in some cases GMG were in apoptosis. The decrease in quantity and size of the granules and the death of GMG might have been caused by the release of the GMG?s granules induced by cytotoxic molecules produced by the protozoan. The death and release of the GMG?s granules might contribute to a premature placental separation and in consequence, to abortion