ArticleThe Journal of infectious diseases2014
Group B Streptococcus β-hemolysin/cytolysin breaches maternal-fetal barriers to cause preterm birth and intrauterine fetal demise in vivo.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled 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.
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.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Prevalence of Group B Streptococcus Recto-Vaginal Colonization, Vertical Transmission, and Antibiotic Susceptibility Among Pregnant Women in Ethiopia: A Systematic Review and Meta-Analysis.Frontiers in public health · 2022Pooled it
- Article
- Microbiota-dependent interferon-λ controls immunity of the uterus and maternal-fetal interface.Research square · 2026Article
- Invasive Streptococcus agalactiae infections in infants in Guangzhou, Southern China (2013-2022): molecular epidemiology and clinical management implications.BMC microbiology · 2026Article
- CRISPR interference in aJournal of bacteriology · 2026Article
- Virulence and pathogenicity of group BVirulence · 2025Review
- Vaginal microbiome and preterm birth: Composition, mechanisms and microbiota‑directed therapies (Review).International journal of molecular medicine · 2025Review
- A Cas12a Toolbox for Rapid and Flexible Group B Streptococcus Genomic Editing and CRISPRi.Molecular microbiology · 2025Article
- Modulation of group BInfection and immunity · 2025Article
- Ascending Vaginal Infection in Mice Induces Preterm Birth and Neonatal Morbidity.The American journal of pathology · 2025Article
- A CRISPRi library screen in group BInfection and immunity · 2025Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- A CRISPRi Library Screen in Group BbioRxiv : the preprint server for biology · 2024Article
- The impact of butyrate on group BInfection and immunity · 2024Article
- Diet influences community dynamics following vaginal group B streptococcus colonization.Microbiology spectrum · 2024Article
- Cerclage prevents ascending intrauterine infection in pregnant mice.American journal of obstetrics and gynecology · 2024Article
- Unlocking the Uterine Code: Microbiota, Immune Cells, and Therapy for Recurrent Reproductive Failure.Microorganisms · 2024Article
- Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota.Nature communications · 2024Article
- Sex-Specific Dysconnective Brain Injuries and Neuropsychiatric Conditions such as Autism Spectrum Disorder Caused by Group BInternational journal of molecular sciences · 2023Review
- Group B Streptococcus Drives Major Transcriptomic Changes in the Colonic Epithelium.Infection and immunity · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMaternal vaginal colonization with Streptococcus agalactiae (Group B Streptococcus [GBS]) is a precursor to chorioamnionitis, fetal infection, and neonatal sepsis, but the understanding of specific factors in the pathogenesis of ascending infection remains limited.
methodsWe used a new murine model to evaluate the contribution of the pore-forming GBS β-hemolysin/cytolysin (βH/C) to vaginal colonization, ascension, and fetal infection.
resultsCompetition assays demonstrated a marked advantage to βH/C-expressing GBS during colonization. Intrauterine fetal demise and/or preterm birth were observed in 54% of pregnant mice colonized with wild-type (WT) GBS and 0% of those colonized with the toxin-deficient cylE knockout strain, despite efficient colonization and ascension by both strains. Robust placental inflammation, disruption of maternal-fetal barriers, and fetal infection were more frequent in animals colonized with WT bacteria. Histopathologic examination revealed bacterial tropism for fetal lung and liver.
conclusionsPreterm birth and fetal demise are likely the direct result of toxin-induced damage and inflammation rather than differences in efficiency of ascension into the upper genital tract. These data demonstrate a distinct contribution of βH/C to GBS chorioamnionitis and subsequent fetal infection in vivo and showcase a model for this most proximal step in GBS pathogenesis.
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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.