The immunobiology of preterm labor and birth: intra-amniotic inflammation or breakdown of maternal-fetal homeostasis

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dc.contributor.authorGomez-Lopez N.
dc.contributor.authorGalaz J.
dc.contributor.authorMiller D.
dc.contributor.authorFarias-Jofre M.
dc.contributor.authorLiu Z.
dc.contributor.authorArenas-Hernandez M.
dc.contributor.authorGarcia-Flores V.
dc.contributor.authorShaffer Z.
dc.contributor.authorGreenberg J.M.
dc.contributor.authorTheis K.R.
dc.contributor.authorRomero R.
dc.date.accessioned2024-01-10T14:25:57Z
dc.date.available2024-01-10T14:25:57Z
dc.date.issued2022
dc.description.abstractIn brief: The syndrome of preterm labor comprises multiple established and novel etiologies. This review summarizes the distinct immune mechanisms implicated in preterm labor and birth and highlights potential strategies for its prevention. Abstract: Preterm birth, the leading cause of neonatal morbidity and mortality worldwide, results from preterm labor, a syndrome that includes multiple etiologies. In this review, we have summarized the immune mechanisms implicated in intra-amniotic inflammation, the best-characterized cause of preterm labor and birth, as well as novel etiologies non-associated with intra-amniotic inflammation (i.e. formally known as idiopathic). While the intra-amniotic inflammatory responses driven by microbes (infection) or alarmins (sterile) have some overlap in the participating cellular and molecular processes, the distinct natures of these two conditions necessitate the implementation of specific approaches to prevent adverse pregnancy and neonatal outcomes. Intra-amniotic infection can be treated with the correct antibiotics, whereas sterile intra-amniotic inflammation could potentially be treated by administering a combination of anti-inflammatory drugs (e.g. betamethasone, inflammasome inhibitors, etc.). Recent evidence also supports the role of fetal T-cell activation as a newly described trigger for preterm labor and birth in a subset of cases diagnosed as idiopathic. Moreover, herein we also provide evidence of two maternally-driven immune mechanisms responsible for preterm births formerly considered to be idiopathic. First, the impairment of maternal Tregs can lead to preterm birth, likely due to the loss of immunosuppressive activity resulting in unleashed effector T-cell responses. Secondly, homeostatic macrophages were shown to be essential for maintaining pregnancy and promoting fetal development, and the adoptive transfer of homeostatic M2-polarized macrophages shows great promise for preventing inflammation-induced preterm birth. Collectively, in this review, we discuss the established and novel immune mechanisms responsible for preterm birth and highlight the potential targets for novel strategies aimed at preventing the multi-etiological syndrome of preterm labor leading to preterm birth.
dc.fuente.origenScopus
dc.identifier.doi10.1530/REP-22-0046
dc.identifier.eissn17417899
dc.identifier.pubmedid35559791
dc.identifier.scopusidSCOPUS_ID:85132454093
dc.identifier.urihttps://doi.org/10.1530/REP-22-0046
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/80388
dc.information.autorucFacultad de Medicina; Farias Jofre, Marcelo Enrique; S/I; 12286
dc.issue.numero2
dc.language.isoen
dc.nota.accesoSin adjunto
dc.publisherNLM (Medline)
dc.relation.ispartofReproduction (Cambridge, England)
dc.revistaReproduction (Cambridge, England)
dc.rightsregistro bibliográfico
dc.titleThe immunobiology of preterm labor and birth: intra-amniotic inflammation or breakdown of maternal-fetal homeostasis
dc.typereseña
dc.volumen164
sipa.codpersvinculados12286
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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