Homeostatic Macrophages Prevent Preterm Birth and Improve Neonatal Outcomes by Mitigating In Utero Sterile Inflammation in Mice

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dc.catalogadorjlo
dc.contributor.authorGarcía-Flores, Valeria
dc.contributor.authorLiu, Zhenjie
dc.contributor.authorRomero, Roberto
dc.contributor.authorPique-Regi, Roger
dc.contributor.authorXu, Yi
dc.contributor.authorMiller, Derek
dc.contributor.authorLevenson, Dustyn
dc.contributor.authorGalaz Alarcón, José Carlo
dc.contributor.authorWinters, Andrew D.
dc.contributor.authorFarias Jofré, Marcelo Enrique
dc.contributor.authorPanzer, Jonathan J.
dc.contributor.authorTheis, Kevin R.
dc.contributor.authorGómez-López, Nardhy
dc.date.accessioned2025-04-15T19:03:06Z
dc.date.available2025-04-15T19:03:06Z
dc.date.issued2024
dc.description.abstractPreterm birth (PTB), often preceded by preterm labor, is a major cause of neonatal morbidity and mortality worldwide. Most PTB cases involve intra-amniotic inflammation without detectable microorganisms, termed in utero sterile inflammation, for which there is no established treatment. In this study, we propose homeostatic macrophages to prevent PTB and adverse neonatal outcomes caused by in utero sterile inflammation. Single-cell atlases of the maternal-fetal interface revealed that homeostatic maternal macrophages are reduced with human labor. M2 macrophage treatment prevented PTB and reduced adverse neonatal outcomes in mice with in utero sterile inflammation. Specifically, M2 macrophages halted premature labor by suppressing inflammatory responses in the amniotic cavity, including inflammasome activation, and mitigated placental and offspring lung inflammation. Moreover, M2 macrophages boosted gut inflammation in neonates and improved their ability to fight systemic bacterial infections. Our findings show that M2 macrophages are a promising strategy to mitigate PTB and improve neonatal outcomes resulting from in utero sterile inflammation.
dc.description.funderEunice Kennedy Shriver National Institute of Child Health and Human Development
dc.description.funderWayne State University Perinatal Initiative in Maternal, Perinatal and Child Health
dc.description.funderNational Institutes of Health
dc.description.funderDivision of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research
dc.description.funderU.S. Department of Health and Human Services
dc.description.funderU.S. Department of Health and Human Services
dc.fuente.origenSCOPUS
dc.identifier.doi10.4049/jimmunol.2400467
dc.identifier.issn1550-6606
dc.identifier.scopusidSCOPUS_ID:85209726802
dc.identifier.urihttps://doi.org/10.4049/jimmunol.2400467
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/103308
dc.information.autorucEscuela de Medicina; Galaz Alarcón, José Carlo; 000-0002-8160-8581; 1034327
dc.information.autorucEscuela de Medicina; Farias Jofré, Marcelo Enrique; 0000-0003-0473-2295; 12286
dc.issue.numero11
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1634
dc.pagina.inicio1620
dc.revistaJournal of Immunology
dc.rightsacceso restringido
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHomeostatic Macrophages Prevent Preterm Birth and Improve Neonatal Outcomes by Mitigating In Utero Sterile Inflammation in Mice
dc.typeartículo
dc.volumen213
sipa.codpersvinculados1034327
sipa.codpersvinculados12286
sipa.trazabilidadSCOPUS;2024-12-08
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