TROPHOBLAST-Trypanosoma cruzi INTERACTION: ROLE

SARTORI MJ; MEZZANO L; REPOSSI G; LIN S; S.P. DE FABRO

Rosario, Sta. Fe

Congreso; - XX Reunión Científica Anual de la Sociedad Argentina de Protozoología; 2004

Sociedad Argentina de Protozoología

Chagas? disease, endemic in 21 countries of Latin America, affectsaround 10 and 20 millions people. One of the infection mechanismsof this disease is the transplacental one. The congenital infectionincidence vary between 1 to 9% of the chagasic pregnantwomen, and the same woman, in different pregnancies, can havechild with our without the disease. As being the Trypanosoma cruzian obligated intracellular parasite, must complete its life cycle in ahost cell, but still now, that process is not well understood. Theparasite adheres to specific receptors on the outer membrane ofhost cells before invasion, inducing changes on the protein patternof the syncitiotrophoblast. Placental alkaline phosphatase (PLAP)(EC 3.1.3.1.), a glycoenzyme anchored to the membrane by a glycosyl-phosphatidylinositol (GPI) molecule, could be solubilized byPhospholipase C (PL-C) and acts as IgG receptor. In this work weobserved that PLAP activity and its presence were altered by theparasite in cocultures of human placental villi and HEp2 cells withT.cruzi, whenever the enzyme was anchored to the membrane byits GPI molecule. The cells treated before the cultures with agentswhich affect PLAP or GPI (antibodies, PL-C, genistein, lithium)presented less parasitic invasion than the control ones. It was alsoobserved a modification in the pattern of actine filaments of thehost cells infected with the protozoo. Thus, it is conclude that PLAPparticipates in the process of T. cruzi invasion into placentalsyncitiotrophoblast cells, by a mechanism that involves hydrolysisof the GPI molecule, the activation of tyrosine kinase proteins, theincrease of cytosolic calcium and finally the rearrangement of actinefilaments of the host cells.