Role of placental alkaline phosphatase in the interaction between human placental trophoblast and Trypanosoma cruzi.

SARTORI MJ, LIN S, FRANK FM, MALCHIODI EL, DE FABRO SP.

EXPERIMENTAL AND MOLECULAR PATHOLOGY.

ACADEMIC PRESS INC ELSEVIER SCIENCE

Lugar: Amsterdam; Año: 2002 vol. 72 p. 84 - 90

0014-4800

Congenital Chagas disease, due to the intracellular parasite Trypanosoma cruzi,is associated with premature labor, miscarriage, and placentitis. Human enzymeplacental alkaline phosphatase (PLAP) (EC 3.1.3.1.) is membrane-anchored through glycosylphosphatidylinositol (GPI). PLAP is present in plasma in late pregnancy, 36 to 40 weeks; there are lower levels in maternal Chagas disease. Infants bornto such mothers may have congenital Chagas disease. Human placental villi (PV)were treated with phospholipase-C (PL-C) and then cultured with T. cruzi todetermine the effect of the parasites on PLAP activity as an in vitro model.There is less PLAP activity after treatment by PL-C and during culture with T.cruzi. Pretreatment of PV with PL-C before culture with T. cruzi yieldedessentially normal specific activity of PLAP and prevented or greatly reducedinfective penetration of villi by parasites. The results are consistent with apathogenetic role for placental alkaline phosphatase in congenital Chagasdisease. Receptor activation of membrane attachment to PLAP may be a device used by T. cruzi to enable parasite invasion of human trophoblast.