ArticleEMBO molecular medicine2015
A streptococcal lipid toxin induces membrane permeabilization and pyroptosis leading to fetal injury.
Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 83 citations in OpenAlex.
- The bacterial cell membrane acts as a dynamic heme reservoir during group BbioRxiv : the preprint server for biology · 2026Article
- Not all Group BFrontiers in cellular and infection microbiology · 2026Article
- Virulence and pathogenicity of group BVirulence · 2025Review
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- 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
- Colonisation of Group BBMJ open · 2023Article
- CD1 and iNKT cells mediate immune responses against the GBS hemolytic lipid toxin induced by a non-toxic analog.PLoS pathogens · 2023Article
- Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy.Molecular systems biology · 2023Article
- Macrophage polarization duringFrontiers in microbiology · 2023Article
- Group B Streptococcus: Virulence Factors and Pathogenic Mechanism.Microorganisms · 2022Review
- The Unequal Impact of the COVID-19 Pandemic on Infant Health.Demography · 2022Article
- Nitric Oxide Production and Effects in Group BPathogens (Basel, Switzerland) · 2022Article
- Mechanisms of group BReproduction & fertility · 2022Review
- Group B Streptococcal Hemolytic Pigment Impairs Platelet Function in a Two-Step Process.Cells · 2022Article
- Genome-Wide CRISPR-Cas9 Screen Does Not Identify Host Factors Modulating Streptococcus agalactiae β-Hemolysin/Cytolysin-Induced Cell Death.Microbiology spectrum · 2022Article
- The pathogenesis of prevalent aerobic bacteria in aerobic vaginitis and adverse pregnancy outcomes: a narrative review.Reproductive health · 2022Review
- MSC-ACE2 AmelioratesFrontiers in immunology · 2022Article
- Pyroptosis: A promising therapeutic target for noninfectious diseases.Cell proliferation · 2021Review
- Hemolytic Membrane Vesicles of Group B Streptococcus Promote Infection.The Journal of infectious diseases · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Group B streptococci (GBS) are Gram-positive bacteria that cause infections in utero and in newborns. We recently showed that the GBS pigment is hemolytic and increased pigment production promotes bacterial penetration of human placenta. However, mechanisms utilized by the hemolytic pigment to induce host cell lysis and the consequence on fetal injury are not known. Here, we show that the GBS pigment induces membrane permeability in artificial lipid bilayers and host cells. Membrane defects induced by the GBS pigment trigger K(+) efflux leading to osmotic lysis of red blood cells or pyroptosis in human macrophages. Macrophages lacking the NLRP3 inflammasome recovered from pigment-induced cell damage. In a murine model of in utero infection, hyperpigmented GBS strains induced fetal injury in both an NLRP3 inflammasome-dependent and NLRP3 inflammasome-independent manner. These results demonstrate that the dual mechanism of action of the bacterial pigment/lipid toxin leading to hemolysis or pyroptosis exacerbates fetal injury and suggest that preventing both activities of the hemolytic lipid is likely critical to reduce GBS fetal injury and preterm birth.
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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.