BECAS
MARVALDI Carolina
congresos y reuniones científicas
Título:
ECs from peripheral blood mononuclear cells is modulated in an LPS-induced preterm murine model
Autor/es:
MARVALDI, CAROLINA; SCHANDER, JULIETA AYLEN; AISEMBERG, JULIETA; FRANCHI, ANA MARIA; WOLFSON, MANUEL LUIS
Reunión:
Congreso; ANNUAL MEETING OF BIOSCIENCE SOCIETIES 2021; 2021
Resumen:
Preterm birth (PTB) is the leading cause ofmortality and morbidity in neonates. The endocannabinoidsystem (ECs) is one of several signaling pathways involved in different aspectsof the physiopathology of reproduction, comprising theenzyme that synthesizes AEA, (N-acylphosphatidylethanolamine-specificphospholipase D, NAPE-PLD), the enzyme that hydrolase AEA (fatty acid amidehydrolase, FAAH), and the receptors CB1, CB2 and TRPV1. Previous works from ourlab have demonstrated that LPS altered FAAH activity in deciduas and PBMC in anembryo resorption model. Using a murine model of preterm labor,induced by two injections of LPS on day 15 of pregnancy, we demonstrated thatECs of the decidua is involved in the triggering of PTB. Due to the decidua ishighly infiltrated by immune cells, in this study we investigated if the ECs ofperipheral blood mononuclear cells (PBMC) is modulated in our LPS-inducedpreterm labor model. Weobserved that CB1 receptor protein levels increased in PBMC after LPS treatment(p<0.05). However, CB2 and TRPV1 receptors protein levels were not modifiedby LPS.  Regardingthe enzyme that synthesizes AEA, (N-acylphosphatidylethanolamine-specificphospholipase D, NAPE-PLD), we observed that its protein levels were diminishedin PBMC from LPS treated mice (p<0.05).  Onthe other hand, the enzyme that degrades AEA(fatty acid amide hydrolase, FAAH) protein levels were diminished inPBMC after LPS treatment (p<0.05). Also, weevaluated FAAH activity by radioconvertion and we observed that FAAH activityis decreased in PBMC from LPS-treated mice.  In summary, these data show that endocannabinoid system fromperipheral blood mononuclear cells could be implicated in the pro-inflammatory responseassociated with LPS-induced preterm birth.