ArticleThe Journal of infectious diseases2021
Hemolytic Membrane Vesicles of Group B Streptococcus Promote Infection.
Article in The Journal of infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges.Infection and immunity · 2026Article
- From biogenesis to host modulation: the expanding biology of oral streptococcal membrane vesicles.FEMS microbiology reviews · 2026Review
- Virulence and pathogenicity of group BVirulence · 2025Review
- Impact of antibiotics on membrane vesicle production in Group BMicrobiology spectrum · 2025Article
- Group B Streptococcal Membrane Vesicles Induce Proinflammatory Cytokine Production and Are Sensed in an NLRP3 Inflammasome-Dependent Mechanism in a Human Macrophage-like Cell Line.ACS infectious diseases · 2025Article
- Cell death in acute lung injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis.Frontiers in pharmacology · 2025Review
- Constitutive activation of two-component systems reveals regulatory network interactions in Streptococcus agalactiae.Nature communications · 2024Article
- Single-Molecule Identification of the Isomers of a Lipidic Antibody Activator.The journal of physical chemistry letters · 2024Article
- An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.FEMS microbiology reviews · 2024Review
- Extracellular vesicles in bacterial and fungal diseases - Pathogenesis to diagnostic biomarkers.Virulence · 2023Review
- Endothelial ADAM10 utilization defines a molecular pathway of vascular injury in mice with bacterial sepsis.The Journal of clinical investigation · 2023Article
- Gram-positive bacterial membrane lipids at the host-pathogen interface.PLoS pathogens · 2023Article
- Group B Streptococcus: Virulence Factors and Pathogenic Mechanism.Microorganisms · 2022Review
- Mechanisms of group BReproduction & fertility · 2022Review
- Yields and Immunomodulatory Effects of Pneumococcal Membrane Vesicles Differ with the Bacterial Growth Phase.Advanced healthcare materials · 2022Article
- Bacterial and Host Determinants of Group B Streptococcal Infection of the Neonate and Infant.Frontiers in microbiology · 2022Review
- Editorial: Streptococci in infectious diseases - pathogenic mechanisms and host immune responses.Frontiers in microbiology · 2022Article
- Production and Composition of Group B Streptococcal Membrane Vesicles Vary Across Diverse Lineages.Frontiers in microbiology · 2021Article
- Bacterial and Host Determinants of Group B Streptococcal Vaginal Colonization and Ascending Infection in Pregnancy.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGroup B streptococci (GBS) are β-hemolytic, Gram-positive bacteria associated with fetal injury, preterm birth, spontaneous abortion, and neonatal infections. A key factor promoting GBS virulence is the β-hemolysin/cytolysin, a pigmented ornithine rhamnolipid (also known as granadaene) associated with the bacterial surface.
methodsA previous study indicated that GBS produce small structures known as membrane vesicles (MVs), which contain virulence-associated proteins. In this study, we show that GBS MVs are pigmented and hemolytic, indicating that granadaene is functionally active in MVs.
resultsIn addition, MVs from hyperhemolytic GBS induced greater cell death of neutrophils, T cells, and B cells compared with MVs from isogenic nonhemolytic GBS, implicating MVs as a potential mechanism for granadaene-mediated virulence. Finally, hemolytic MVs reduced oxidative killing of GBS and aggravated morbidity and mortality of neonatal mice infected with GBS.
conclusionsThese studies, taken together, reveal a novel mechanism by which GBS deploy a crucial virulence factor to promote bacterial dissemination and pathogenesis.
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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.