Table 2.

Compilation of studies where human placental explants have been employed to study host-parasite interactions ex vivo.

Parasite used for infection	Main findings in human placental explants	References
T. gondii	Infection induces the secretion of the macrophage migration inhibitory factor (MIF), up-regulates ICAM-1 expression, and increases monocyte adhesiveness to trophoblast	(149)
	Parasite burdens are determined by the expression of MIF receptors and its secretion, which varies with the trimester of gestation	(150)
	The extravillous trophoblasts (fetal) are preferentially colonized over the syncytiotrophoblast (maternal), which is linked to an up-regulation of the chemoattractant CCL22	(151, 152)
	Parasite proliferation relies on iron acquirement from the placenta	(153)
	Azithromycin, enrofloxacin or toltrazuril modulate MIF production by explants and reduce parasite replication	(145, 154, 155)
	Infection inhibits the non-canonical NF-κB pathway through TLR-4 and TLR-9 related mechanisms, resulting in higher parasite burdens	(156, 157)
T. cruzi	The syncytiotrophoblast (maternal placenta) limits infection through the production of nitric oxide	(158–160)
	Infection induces trophoblast differentiation, tissue disorganization, destruction of chorionic villi and apoptosis	(160–164)
	TLR-2 activation and the NF-κB pathway are key to control infection	(156, 157, 165)
P. falciparum	Infection alters the Th2 bias of maternal immunity and elicits a Th1 response	(166, 167)