ArticleJCI insight2020
Maternal regulation of inflammatory cues is required for induction of preterm birth.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
The trial behind it
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Who cites it
29 citing papers in PubMed, 31 citations in OpenAlex.
- AAT/SERPINA1 Pi*Z variant linked to gestational length and preterm birth prevention via AAT in mice.Nature communications · 2026Article
- Ambient temperature regulates CD4iScience · 2026Article
- The Pathophysiology of Spontaneous Preterm Birth: Emerging Mechanisms Reviewed by the Preterm Birth International Collaborative.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Artemin Serves as a Novel Predictive Biomarker and Exerts a Protective Effect Against Preterm Birth.Journal of inflammation research · 2026Article
- A systematic scoring system to optimise the testing of neurotherapeutics in models of perinatal brain injury, with an applied case study of human umbilical-cord MSC.Journal of neuroinflammation · 2025Article
- Article
- N,N-dimethylacetamide blocks inflammation-induced preterm birth and remediates maternal systemic immune responses.Scientific reports · 2025Article
- N,N-dimethylacetamide blocks inflammation-induced preterm birth and remediates maternal systemic immune responses.bioRxiv : the preprint server for biology · 2025Article
- Dynamic changes in the pregnancy microbiome and their role in preterm birth.Frontiers in cellular and infection microbiology · 2025Review
- Predictors of Inflammation-Mediated Preterm Birth.Physiology (Bethesda, Md.) · 2025Review
- Biological and behavioral pathways from prenatal depression to offspring cardiometabolic risk: Testing the developmental origins of health and disease hypothesis.Developmental psychology · 2024Review
- Deciphering maternal-fetal cross-talk in the human placenta during parturition using single-cell RNA sequencing.Science translational medicine · 2024Article
- Deciphering a critical role of uterine epithelial SHP2 in parturition initiation at single cell resolution.Nature communications · 2023Article
- Stromal cells-specific retinoic acid determines parturition timing at single-cell and spatial-temporal resolution.iScience · 2023Article
- A key role for NLRP3 signaling in preterm labor and birth driven by the alarmin S100B.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Emerging role of toll-like receptors signaling and its regulators in preterm birth: a narrative review.Archives of gynecology and obstetrics · 2023Review
- Maternal Vaccination to Prevent Adverse Pregnancy Outcomes: An Underutilized Molecular Immunological Intervention?Journal of molecular biology · 2023Review
- BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth.Cell reports · 2023Article
- Elevated expression of Toll-like receptor 4 and cytokines in both serum and myometrium at term may serve as promising biomarkers for uterine activation preceding labor.Frontiers in endocrinology · 2023Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Infection-driven inflammation in pregnancy is a major cause of spontaneous preterm birth (PTB). Both systemic infection and bacterial ascension through the vagina/cervix to the amniotic cavity are strongly associated with PTB. However, the contribution of maternal or fetal inflammatory responses in the context of systemic or localized models of infection-driven PTB is not well defined. Here, using intraperitoneal or intraamniotic LPS challenge, we examined the necessity and sufficiency of maternal and fetal Toll-like receptor (TLR) 4 signaling in induction of inflammatory vigor and PTB. Both systemic and local LPS challenge promoted induction of inflammatory pathways in uteroplacental tissues and induced PTB. Restriction of TLR4 expression to the maternal compartment was sufficient for induction of LPS-driven PTB in either systemic or intraamniotic challenge models. In contrast, restriction of TLR4 expression to the fetal compartment failed to induce LPS-driven PTB. Vav1-Cre-mediated genetic deletion of TLR4 suggested a critical role for maternal immune cells in inflammation-driven PTB. Further, passive transfer of WT in vitro-derived macrophages and dendritic cells to TLR4-null gravid females was sufficient to induce an inflammatory response and drive PTB. Cumulatively, these findings highlight the critical role for maternal regulation of inflammatory cues in induction of inflammation-driven parturition.
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What OpenQuestion holds
Registered trials
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.