Betamethasone as a potential treatment for preterm birth associated with sterile intra-amniotic inflammation: a murine study

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dc.contributor.authorGalaz, Jose
dc.contributor.authorRomero, Roberto
dc.contributor.authorArenas-Hernandez, Marcia
dc.contributor.authorPanaitescu, Bogdan
dc.contributor.authorPara, Robert
dc.contributor.authorGomez-Lopez, Nardhy
dc.date.accessioned2025-01-20T22:08:30Z
dc.date.available2025-01-20T22:08:30Z
dc.date.issued2021
dc.description.abstractObjectives: Preterm birth remains the leading cause of perinatal morbidity and mortality worldwide. Preterm birth is preceded by spontaneous preterm labor, which is commonly associated with sterile intra-amniotic inflammation; yet, no approved treatment exists for this clinical condition. Corticosteroids are the standard of care to improve neonatal outcomes in women at risk of preterm birth. Herein, we first validated our model of alarmininduced preterm birth. Next, we investigated whether treatment with betamethasone could prevent preterm birth resulting from sterile intra-amniotic inflammation in mice.
dc.description.abstractMethods: Under ultrasound guidance, the first cohort of dams received an intra-amniotic injection of the alarmin high-mobility group box-1 (HMGB1, n=10) or phosphatebuffered saline (PBS, n=9) as controls. A second cohort of dams received HMGB1 intra-amniotically and were subcutaneously treated with betamethasone (n=15) or vehicle (n=15). Dams were observed until delivery, and perinatal outcomes were observed.
dc.description.abstractResults: Intra-amniotic HMGB1 reduced gestational length (p=0.04), inducing preterm birth in 40% (4/10) of cases, of which 100% (4/4) were categorized as late preterm births. Importantly, treatment with betamethasone extended the gestational length (p=0.02), thereby reducing the rate of preterm birth by 26.6% (from 33.3% [5/15] to 6.7% [1/15]). Treatment with betamethasone did not worsen the rate of neonatal mortality induced by HMGB1 or alter weight gain in the first three weeks of life.
dc.description.abstractConclusions: Treatment with betamethasone prevents preterm birth induced by the alarmin HMGB1. This study supports the potential utility of betamethasone for treating women with sterile intra-amniotic inflammation.
dc.fuente.origenWOS
dc.identifier.doi10.1515/jpm-2021-0049
dc.identifier.eissn1619-3997
dc.identifier.issn0300-5577
dc.identifier.urihttps://doi.org/10.1515/jpm-2021-0049
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/94297
dc.identifier.wosidWOS:000695645000018
dc.issue.numero7
dc.language.isoen
dc.pagina.final906
dc.pagina.inicio897
dc.revistaJournal of perinatal medicine
dc.rightsacceso restringido
dc.subjectalarmins
dc.subjectantenatal corticosteroids
dc.subjecthigh-mobility group box-1 (HMGB1)
dc.subjectpregnancy
dc.subjectprematurity
dc.subjectpretermlabor
dc.subject.ods03 Good Health and Well-being
dc.subject.ods05 Gender Equality
dc.subject.odspa03 Salud y bienestar
dc.subject.odspa05 Igualdad de género
dc.titleBetamethasone as a potential treatment for preterm birth associated with sterile intra-amniotic inflammation: a murine study
dc.typeartículo
dc.volumen49
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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