IQUIBICEN   23947
INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CIENCIAS EXACTAS Y NATURALES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Trophoblast cells regulate immune cell functional profile through VIP-mediated pathways
Autor/es:
D. PAPARINI, G. CALO, V. HAUK, F. MERECH, R. RAMHORST, C. PEREZ LEIROS.
Lugar:
Puerto Varas
Reunión:
Congreso; Latin American Society for Maternal Fetal Interaction.; 2017
Resumen:
Deep placentation disorders such as pre-eclampsia are associated with loss of immune homeostasis. Maternal leukocytes are recruited to the maternal-placental interface from the beginning of pregnancy and both normal placentation and the success of pregnancy highly depends on an appropriate communication established with trophoblast cells. From an immunological point of view, normal placentation is associated with the maintenance of immune homeostasis through redundant loops of cell-to-cell interaction as well as the local release of mediators to sustain an anti-inflammatory microenvironment. Among those factors we have proposed the vasoactive intestinal peptide (VIP) and its high affinity receptors VPAC to have a central role. Objective: To explore the relevance of trophoblast VIP at the early maternal-placental interface and its impact on trophoblast function and interaction with immune cells.Methods: Trophoblast cell lines Sawn 71 and HTR8 were silenced in VIP expression with siRNA of VIP at two concentrations or with an irrelevant siRNA as a control. Blood monocytes or neutrophils from healthy donors were co-cultures with trophoblast cells or cell conditioned media and immune and trophoblast cell functional markers were assessed. Results: We present evidence to indicate that VIP deficient trophoblast cells fail to promote a predominant M2 macrophage polarization profile, as well as to deactivate neutrophils primed with pro-inflammatory stimuli. Conclusions: We propose that the loss of immune homeostasis at the maternal-placental interface is triggered by an impaired trophoblast migration and invasion associated with a defective activation of VIP/VPAC system that fails to modulate both trophoblast function and trophoblast-immune interaction.