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:
DANIEL PAPARINI; FATIMA MERECH; GUILLERMINA CALO; ROSANNA RAMHORST; DAIANA VOTA; VANESA HAUK; CLAUDIA PEREZ LEIROS
Reunión:
Congreso; Congreso de la Sociedad Latinoamericana de Interacción Materno-Fetal y Placenta; 2017
Resumen:
Deep placentation disorders such as preeclampsia are associated with lossof immune homeostasis. Maternal leukocytes are recruited to thematernal-placental interface from the beginning of pregnancy and bothnormal placentation and the success of pregnancy strongly depend on anappropriate communication established with trophoblast cells. From animmunological standpoint, normal placentation is associated with themaintenance of immune homeostasis through redundant loops of cell-tocellinteraction as well as the local release of mediators to sustain an antiinflammatorymicroenvironment. Among those factors we have proposedthe vasoactive intestinal peptide (VIP) and its high affinity receptors VPACto have a central role.Objective: To explore the relevance of trophoblast cell VIP at the earlymaternal-placental interface as well as its impact on trophoblast functionand interaction with immune cells.Methods: Trophoblast derived cell lines Swan 71 and HTR8 were transfectedwith a VIP siRNA to knock down its expression or with an irrelevantsiRNA as a control. Blood monocytes or neutrophils from healthy donorswere co-cultured with trophoblast cells or their conditioned media andimmune and trophoblast cell functional profiles were assessed.Results: VIP deficient trophoblast cells exhibited an impaired migrationand failed to promote an M2 macrophage profile, as well as to deactivateneutrophils primed with pro-inflammatory stimuli.Conclusions: Results support that the loss of immune homeostasis at thematernal-placental interface involves an impaired trophoblast migrationand invasion associated with a defective activation of VIP/VPAC systemthat fails to modulate both trophoblast function and trophoblast-immuneinteraction.