INVESTIGADORES
FERRERO Mariana Cristina
congresos y reuniones científicas
Título:
Impact of Brucella abortus and B. melitensis infection on the innate immune response and the release of extracellular vesicles by the placenta
Autor/es:
ZAVATTIERI LUCÍA; SPILBARG NATALIA; GARCIA MARIA NOE; GRASSO DANIEL; FLORENCIA MUÑOZ GONZALEZ; BALDI PABLO C; FERRERO MARIANA CRISTINA
Lugar:
San Luis
Reunión:
Congreso; LXXI Reunion Anual de la Sociedad Argentina de Inmunología; 2023
Institución organizadora:
Sociedad Argentina de Inmunología
Resumen:
Impact of Brucella abortus and B. melitensis infection on the innate immune response and the release of extracellular vesicles by the placenta.Lucia Zavattieri 1, Natalia Szpilbarg 2, Maria Noe Garcia 1, Daniel Grasso 1, Florencia Muñoz González 1, Pablo C Baldi 1, Mariana C Ferrero 1.1 IDEHU (CONICET-UBA), Facultad de Farmacia y Bioquímica UBA, Buenos Aires, Argentina; 2 IFIBIO- CONICET- Facultad de Medicina, UBA, Buenos Aires, Argentina. Placental immunity is crucial for fetal well-being in pregnancy, since invading pathogens can be transmitted from the maternal blood to the fetus through this organ. However, excessive inflammatory responses in the placenta can be detrimental to both the fetus and the pregnant mother. Placental extracellular vesicles (pEV) are generated by trophoblasts and regulate immunological tolerance towards the fetus and the placenta itself. Brucella infection has been associated with reproductive complications in humans and animals, and inflammation has been shown to be involved. In this study, we investigated the impact of B. abortus and B. melitensis infection on the innate immune response of the placenta and the production of placental pEV. To do so, we utilized an ex vivo infection model of explants from human placenta at term. “Small pEV” were isolated by ultracentrifugation of culture supernatants from infected and uninfected explants at 18 h post-infection (p.i.). Our findings demonstrated that infection with B. abortus and B. melitensis induces significant increases in CCL2 (p