ReviewClinical & translational immunology2020
Targeting Toll-like receptor-4 to tackle preterm birth and fetal inflammatory injury.
Review in Clinical & translational immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Molecular Mechanism and Pathways of Spontaneous Preterm Birth in Different Gestational Tissues: A Systematic Review of Transcriptome Studies.International journal of molecular sciences · 2026Pooled it
- A systematic review of immune-based interventions for perinatal neuroprotection: closing the gap between animal studies and human trials.Journal of neuroinflammation · 2023Pooled it
- Impact of Extreme Prematurity, Chorioamnionitis, and Sepsis on Neonatal Monocyte Characteristics and Functions.Journal of innate immunity · 2024Trial
- The central function and specific molecular mechanisms of the TLR4 pathway underlying impaired intestinal barrier in necrotizing enterocolitis.Biochemistry and biophysics reports · 2026Review
- Targeting NF-κB Signaling in Preterm Labor: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Immunology of pregnancy and sepsis: shared and specific pathways guiding future precision care.EBioMedicine · 2026Review
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- Gut-placenta axis: gut microbiota metabolites may play a role in regulating maternal-fetal immune tolerance and the pathogenesis of adverse pregnancy outcomes.Frontiers in immunology · 2026Review
- A model of early-life interactions between the gut microbiome and adaptive immunity provides insights into the ontogeny of immune tolerance.PLoS biology · 2025Article
- Impact of Sociodemographic, Clinical, and Genetic Factors andIranian journal of medical sciences · 2025Article
- Review
- TLR2 and TLR4 bridge physiological and pathological inflammation in the reproductive system.Communications biology · 2025Review
- IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.Cell communication and signaling : CCS · 2025Article
- Interaction of vaginal microbiota and biomarkers in Premature rupture of membranes: from bench to beside.Frontiers in immunology · 2025Review
- The Immunomodulatory Role of Regulatory T Cells in Preterm Birth and Associated Pregnancy Outcomes.International journal of molecular sciences · 2024Review
- Escherichia coli induced matrix metalloproteinase-9 activity and type IV collagen degradation is regulated by progesterone in human maternal decidual.BMC pregnancy and childbirth · 2024Article
- The relationship between Toll-like receptor-4 genes and preeclampsia outcomes.Journal of assisted reproduction and genetics · 2024Article
- BKCa channels are involved in spontaneous and lipopolysaccharide-stimulated uterine contraction in late gestation mice†.Biology of reproduction · 2024Article
- Dysbiotic Vaginal Microbiota Induces Preterm Birth Cascade via Pathogenic Molecules in the Vagina.Metabolites · 2024Article
- Developmental outcomes with perinatal exposure (DOPE) to prescription opioids.NeuroImmune pharmacology and therapeutics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Every year, 15 million pregnancies end prematurely, resulting in more than 1 million infant deaths and long-term health consequences for many children. The physiological processes of labour and birth involve essential roles for immune cells and pro-inflammatory cytokines in gestational tissues. There is compelling evidence that the mechanisms underlying spontaneous preterm birth are initiated when a premature and excessive inflammatory response is triggered by infection or other causes. Exposure to pro-inflammatory mediators is emerging as a major factor in the 'fetal inflammatory response syndrome' that often accompanies preterm birth, where unscheduled effects in fetal tissues interfere with normal development and predispose to neonatal morbidity. Toll-like receptors (TLRs) are critical upstream gatekeepers of inflammatory activation. TLR4 is prominently involved through its ability to sense and integrate signals from a range of microbial and endogenous triggers to provoke and perpetuate inflammation. Preclinical studies have identified TLR4 as an attractive pharmacological target to promote uterine quiescence and protect the fetus from inflammatory injury. Novel small-molecule inhibitors of TLR4 signalling, specifically the non-opioid receptor antagonists (+)-naloxone and (+)-naltrexone, are proving highly effective in animal models for preventing preterm birth induced by bacterial mimetic LPS, heat-killed
Indexed as
Identifiers
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.