TROPHOBLAST-MONOCYTE/MACROPHAGE INTERACTION ELICITS BIDIRECTIONAL METABOLIC REPROGRAMMING

FATIMA MERECH ; SOLEDAD GORI; GRACIELA REYSCHER; DANIEL PAPARINI; VANESA HAUK; MARIELA VIDELA; MARIELA GARCIA; ROSANNA RAMHORST; MARIA EUGENIA MONGE; DAIANA VOTA ; CLAUDIA PÉREZ LEIRÓS

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias SAIC-SAI 2022; 2022

SAI-SAIC-SAFIS

Bidirectional interaction of trophoblast cells (Tb) and maternal leukocytes support homeostasis maintenance at placentation. Tb modulate decidual macrophages to an anti-inflammatory profile throughcytokines and other factors released. Both Tb and macrophages display highly active metabolism to adapt to variable nutrient and oxygen placental microenvironments. However, a role for metabolitesas mediators in the trophoblast-macrophage interaction is unclear,entailing a new research area within Immunometabolism sustainedon novel metabolomics approaches. We have shown that the conditioned media of Tb (Tb-CM) prevent LPS-induced glucose uptakein monocytes/macrophages (CD14+) and promote anti-inflammatory markers. Here we studied the trophoblast-CD14+ cell metabolicrewiring upon in vitro interaction. Monocytes were isolated from peripheral blood of female donors byPercoll. M1 macrophages were obtained after differentiation 5+2days with GM-CSF and E. coli LPS; M1 conditioned media (M1-CM)collected in RPMI-FBS 2% 24h later. Tb metabolism was studied inthe human trophoblast cell line Swan-71. Tb-CM was collected after 18h. Glucose, long chain polyunsaturated fatty acids (LCPUFAs)uptake and lipid droplets were evaluated using D-glucose analog(2-NBDG), Bodipy FL C12 or 493/503 respectively by flow cytometry, and gene expression by RT-qPCR. Proinflammatory M1-CM induced rapid (4h) glucose uptake in Tb and increased cell migration.However, it decreased TNFa and IL1b (p