Evidence map›Paper›PMID 42379806›Full record

ArticleIn vivo (Athens, Greece)

Time-Dependent Inflammatory Cytokine Responses in a Human Fetal Membrane Dual-Compartment Model.

Katharina Sterenczak, Yasmin Engist, Luise Koepke, Marina Polei, Hans-Juergen Kreutzer, Hugo Murua Escobar, Johannes Stubert

Abstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Katharina SterenczakDepartment of Obstetrics and Gynecology, Rostock University Medical Center, Rostock, Germany; katharina.sterenczak@kliniksued-rostock.de.
Yasmin EngistDepartment of Obstetrics and Gynecology, Rostock University Medical Center, Rostock, Germany.
Luise KoepkeDepartment of Obstetrics and Gynecology, Rostock University Medical Center, Rostock, Germany.
Marina PoleiDepartment of Obstetrics and Gynecology, Rostock University Medical Center, Rostock, Germany.
Hans-Juergen KreutzerInstitute of Pathology, Suedstadt Hospital, Rostock, Germany.
Hugo Murua EscobarInstitute and Outpatient Clinic of Medical Genetics, Rostock University Medical Center, Rostock, Germany.
Johannes StubertDepartment of Obstetrics and Gynecology, Rostock University Medical Center, Rostock, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimPreterm birth is a leading cause of neonatal morbidity and mortality, with inflammation at the feto-maternal interface playing a central role in its pathogenesis. Human fetal membrane models provide a physiologically relevant platform to investigate inflammatory mechanisms and evaluate targeted interventions. MATERIALS AND

methodsHuman fetal membrane explants from term cesarean deliveries were cultured in a dual-compartment system enabling side-specific stimulation and compartment-resolved analysis. Inflammation was induced by amniotic application of lipopolysaccharide (LPS; 1,000-10,000 ng/ml), and interleukin (IL)-1β and IL-6 concentrations were quantified over 1-48 h. Rytvela (0.1-10 μM), an allosteric IL-1 receptor modulator, was evaluated in a subset of experiments using preceding, simultaneous, and delayed administration relative to LPS exposure.

resultsLPS induced time- and dose-dependent increases in IL-1β and IL-6. IL-6 responses were detectable from 6 h onward, whereas IL-1β increased at later time points (24-48 h). Rytvela alone did not induce cytokine secretion. Modulation of IL-1β responses differed between treatment regimens: while IL-1β levels were increased across all LPS-containing conditions, preceding rytvela was associated with comparatively lower IL-1β levels than simultaneous or delayed administration. In contrast, IL-6 levels were not consistently affected by rytvela across experimental conditions.

conclusionThe dual-compartment fetal membrane model enables time-resolved analysis of inflammatory responses under physiologically relevant conditions. Preceding administration of rytvela was associated with lower IL-1β levels compared to simultaneous or delayed treatment, whereas IL-6 responses were not consistently affected. These findings suggest that timing and pathway-specific regulation may influence inflammatory responses in fetal membranes.

Indexed as

CytokinesExtraembryonic MembranesInflammationInflammation MediatorsFemaleHumansInterleukin-1betaInterleukin-6LipopolysaccharidesModels, BiologicalPregnancyPremature BirthTime FactorsCytokinesInflammation MediatorsInterleukin-1betaInterleukin-6Lipopolysaccharidescytokinesex vivo modelfetal membranesintra-amniotic inflammationPreterm birthrytvela

Identifiers

PMID42379806
PMCPMC13321942

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.