Fetal and maternal NLRP3 signaling is required for preterm labor and birth

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dc.contributor.authorMotomura, Kenichiro
dc.contributor.authorRomero, Roberto
dc.contributor.authorGalaz, Jose
dc.contributor.authorTao, Li
dc.contributor.authorGarcia-Flores, Valeria
dc.contributor.authorXu, Yi
dc.contributor.authorDone, Bogdan
dc.contributor.authorArenas-Hernandez, Marcia
dc.contributor.authorMiller, Derek
dc.contributor.authorGutierrez-Contreras, Pedro
dc.contributor.authorFarias-Jofre, Marcelo
dc.contributor.authorAras, Siddhesh
dc.contributor.authorGrossman, Lawrence, I
dc.contributor.authorTarca, Adi L.
dc.contributor.authorGomez-Lopez, Nardhy
dc.date.accessioned2024-01-10T13:10:38Z
dc.date.available2024-01-10T13:10:38Z
dc.date.issued2022
dc.description.abstractPreterm birth is the leading cause of neonatal morbidity and mortality worldwide. One of every 4 preterm neonates is born to a mother with intra-amniotic inflammation driven by invading bacteria. However, the molecular mechanisms underlying this hostile immune response remain unclear. Here, we used a translationally relevant model of preterm birth in Nlrp3-deficient and-sufficient pregnant mice to identify what we believe is a previously unknown dual role for the NLRP3 pathway in the fetal and maternal signaling required for the premature onset of the labor cascade leading to fetal injury and neonatal death. Specifically, the NLRP3 sensor molecule and/or inflammasome is essential for triggering intra-amniotic and decidual inflammation, fetal membrane activation, uterine contractility, and cervical dilation. NLRP3 also regulates the functional status of neutrophils and macrophages in the uterus and decidua, without altering their influx, as well as maternal systemic inflammation. Finally, both embryo transfer experimentation and heterozygous mating systems provided mechanistic evidence showing that NLRP3 signaling in both the fetus and the mother is required for the premature activation of the labor cascade. These data provide insights into the mechanisms of fetal-maternal dialog in the syndrome of preterm labor and indicate that targeting the NLRP3 pathway could prevent adverse perinatal outcomes.
dc.fechaingreso.objetodigital2024-05-07
dc.fuente.origenWOS
dc.identifier.doi10.1172/jci.insight.158238
dc.identifier.eissn2379-3708
dc.identifier.urihttps://doi.org/10.1172/jci.insight.158238
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/77899
dc.identifier.wosidWOS:000844659700001
dc.information.autorucFacultad de Medicina; Farias Jofre, Marcelo Enrique; S/I; 12286
dc.issue.numero16
dc.language.isoen
dc.nota.accesoSin adjunto
dc.publisherAMER SOC CLINICAL INVESTIGATION INC
dc.revistaJCI INSIGHT
dc.rightsregistro bibliográfico
dc.subject.ods05 Gender Equality
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa05 Igualdad de género
dc.subject.odspa03 Salud y bienestar
dc.titleFetal and maternal NLRP3 signaling is required for preterm labor and birth
dc.typeartículo
dc.volumen7
sipa.codpersvinculados12286
sipa.indexWOS
sipa.trazabilidadCarga SIPA;09-01-2024
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