Trypanosoma cruzi-derived exovesicles contribute to parasite infection, tissue damage, and apoptotic cell death during ex vivo infection of human placental explants
Metadatos
Mostrar el registro completo del ítemAutor
Fernández-Moya, Alejandro; Oviedo, Bielca; Liempi, Ana; Guerrero Muñóz, Jesús; Rivas, Cristian; Arregui, Roc; Araneda, Sebastian; Cornet Gómez, Alberto; Maya, Juan Diego; Müller, Marioly; Osuna Carrillo De Albornoz, Antonio; Castillo, Christian; Kemmerling, UlrikeEditorial
Frontiers Media
Materia
Trypanosoma cruzi placenta tissue damage infection exovesicles
Fecha
2024-10-14Referencia bibliográfica
Fernández Moya, A. et. al. Front. Cell. Infect. Microbiol. 14:1437339. [https://doi.org/10.3389/fcimb.2024.1437339]
Patrocinador
National Fund for Scientific and Technological Development (FONDECYT; grant numbers 1220105, 1210159, and 11220310, respectively); PhD scholarship from the same agency (Beca ANID 21201823)Resumen
Trypanosoma cruzi, the causative agent of Chagas disease, can be congenitally
transmitted by crossing the placental barrier. This study investigates the role of T.
cruzi-derived exovesicles (TcEVs) in facilitating parasite infection and the
consequent tissue damage and apoptotic cell death in human placental
explants (HPEs). Our findings demonstrate that TcEVs significantly enhance the
parasite load and induce tissue damage in HPEs, both in the presence and
absence of the parasite. Through histopathological and immunohistochemical
analyses, we show that TcEVs alone can disrupt the placental barrier, affecting
the basal membrane and villous stroma. The induction of apoptotic cell death is
evidenced by DNA fragmentation, caspase 8 and 3, and p18 fragment
immunodetection. This damage is exacerbated when TcEVs are combined with
T. cruzi infection. These findings suggest that TcEVs play a critical role in the
pathogenesis of congenital Chagas disease by disrupting the placental barrier
and facilitating parasite transmission to the fetus. This study provides new insights
into the mechanisms of transplacental transmission of T. cruzi and highlights the
potential of targeting TcEVs as a therapeutic strategy against congenital
Chagas disease.