Evidence map›Paper›PMID 42606825›Full record

ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2026

Interleukin-1 Receptor Accessory Protein Amplifies Trophoblast Inflammatory Signaling in Inflammation-Associated Preterm Birth.

Jasmine Edghill, Busra Cetinkaya-Un, Jessica Lynch, Burak Un, Isabella Hetherington, Md Abu Rahat, Marian Kacerovsky, Charles J Lockwood, Ozlem Guzeloglu-Kayisli, Hana Totary-Jain

Abstract read
In one paragraph

Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2026. 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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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

10 authors.

Jasmine EdghillDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Busra Cetinkaya-UnDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Jessica LynchDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Burak UnDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.ORCID https://orcid.org/0000-0002-8885-7062
Isabella HetheringtonDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.ORCID https://orcid.org/0000-0001-7197-5241
Md Abu RahatDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.ORCID https://orcid.org/0009-0000-8065-1046
Marian KacerovskyDepartment of Obstetrics and Gynecology, University Hospital Olomouc, Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech Republic.
Charles J LockwoodDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Ozlem Guzeloglu-KayisliDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.ORCID https://orcid.org/0000-0001-5448-917X
Hana Totary-JainDepartment of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.ORCID https://orcid.org/0000-0003-2203-0377

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

problemInflammation contributes to spontaneous preterm birth, yet mechanisms regulating trophoblast inflammatory responsiveness remain unclear. Interleukin-1 beta (IL1β) is a potent mediator of labor-associated inflammation, but the role of its accessory receptor, IL-1 receptor accessory protein (IL-1RAP), at the maternal-fetal interface is poorly understood. METHOD OF STUDY: IL-1RAP expression and localization were assessed in preterm chorioamniotic membranes with or without intra-amniotic inflammation. Decidual regulation of trophoblast IL1RAP was evaluated in primary trophoblasts, and gain- and loss-of-function studies in HTR8/SV

resultsIL1RAP expression was increased in fetal membranes from inflammation-associated preterm labor and IL-1RAP localized prominently to extravillous trophoblasts. Decidual cell-conditioned media increased trophoblast IL1RAP expression. IL1RAP overexpression enhanced basal and IL-1β-induced expression of inflammatory mediators, including TNF, IL1B, IL6, and CXCL8/IL8, whereas IL1RAP silencing most consistently attenuated IL-1β-induced TNF expression.

conclusionsThese findings identify trophoblast IL-1RAP as an amplifier of IL-1β-mediated inflammatory signaling and support further investigation of IL-1RAP in inflammation-associated preterm birth.

Indexed as

InflammationInterleukin-1 Receptor Accessory ProteinPremature BirthTrophoblastsCell LineDeciduaExtravillous TrophoblastsFemaleHumansInterleukin-1betaPregnancySignal TransductionIL1RAP protein, humanInterleukin-1betaInterleukin-1 Receptor Accessory Proteinfetal membranesIL‐1β signalinginflammatory signalinginterleukin‐1 receptor accessory proteinintra‐amniotic inflammationmaternal‐fetal interfacepreterm birthtrophoblast

Identifiers

PMID42606825
PMCPMC13480343

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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.