ArticlePLoS pathogens2011
Glycosaminoglycan binding facilitates entry of a bacterial pathogen into central nervous systems.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed.
- CCHFV GP38 and GP85 interact with cell-surface glycosaminoglycans.Npj viruses · 2026Article
- Aminopeptidase M17 in bacteria: insights into structure, function, and potential as a drug target.Journal of bacteriology · 2026Review
- Group B Streptococci lyse endothelial cells to infect the brain in a zebrafish meningitis model.PLoS biology · 2025Article
- Pathogens that infect mammalian cells via sulfonated glycosaminoglycans.Frontiers in cellular and infection microbiology · 2025Review
- Glycan-mediated adhesion mechanisms in antibiotic-resistant bacteria.BBA advances · 2025Article
- The pathways and the mechanisms by whichMycology · 2024Review
- Respiratory viruses interacting with cells: the importance of electrostatics.Frontiers in microbiology · 2023Review
- Heparan Sulfate Glycosaminoglycans: (Un)Expected Allies in Cancer Clinical Management.Biomolecules · 2021Review
- The Unifying Hypothesis of Alzheimer's Disease: Heparan Sulfate Proteoglycans/Glycosaminoglycans Are Key as First Hypothesized Over 30 Years Ago.Frontiers in aging neuroscience · 2021Article
- Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption.Virulence · 2020Article
- Heparin Inhibits Cellular Invasion by SARS-CoV-2: Structural Dependence of the Interaction of the Spike S1 Receptor-Binding Domain with Heparin.Thrombosis and haemostasis · 2020Article
- An original infection model identifies host lipoprotein import as a route for blood-brain barrier crossing.Nature communications · 2020Article
- Article
- Review
- Heparan Sulfate Proteoglycans as Relays of Neuroinflammation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis.Virulence · 2018Article
- Innate immune evasion strategies against Cryptococcal meningitis caused byExperimental and therapeutic medicine · 2017Article
- Zinc metalloproteinase ZmpC suppresses experimental pneumococcal meningitis by inhibiting bacterial invasion of central nervous systems.Virulence · 2017Article
- New Applications of Heparin and Other Glycosaminoglycans.Molecules (Basel, Switzerland) · 2017Review
- Glycosaminoglycans are involved in bacterial adherence to lung cells.BMC infectious diseases · 2017Article
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.
Funding
Abstract
Certain microbes invade brain microvascular endothelial cells (BMECs) to breach the blood-brain barrier (BBB) and establish central nervous system (CNS) infection. Here we use the leading meningitis pathogen group B Streptococcus (GBS) together with insect and mammalian infection models to probe a potential role of glycosaminoglycan (GAG) interactions in the pathogenesis of CNS entry. Site-directed mutagenesis of a GAG-binding domain of the surface GBS alpha C protein impeded GBS penetration of the Drosophila BBB in vivo and diminished GBS adherence to and invasion of human BMECs in vitro. Conversely, genetic impairment of GAG expression in flies or mice reduced GBS dissemination into the brain. These complementary approaches identify a role for bacterial-GAG interactions in the pathogenesis of CNS infection. Our results also highlight how the simpler yet genetically conserved Drosophila GAG pathways can provide a model organism to screen candidate molecules that can interrupt pathogen-GAG interactions for future therapeutic applications.
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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.