ArticleThe Journal of biological chemistry2014
The role of autophagy during group B Streptococcus infection of blood-brain barrier endothelium.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Protective effects of metabolites from lactic acid bacteria against infections of mastitis pathogen in bovine cells.Scientific reports · 2025Article
- Group B Streptococci lyse endothelial cells to infect the brain in a zebrafish meningitis model.PLoS biology · 2025Article
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Unveiling the crucial role of ferroptosis in host resistance to streptococcus agalactiae infection.Cell death discovery · 2024Article
- Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes.Biomedicines · 2023Article
- Pathogenic bacteria exploit transferrin receptor transcytosis to penetrate the blood-brain barrier.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Membrane vesicle delivery of a streptococcal M protein disrupts the blood-brain barrier by inducing autophagic endothelial cell death.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Membrane Vesicles Derived from Gut Microbiota and Probiotics: Cutting-Edge Therapeutic Approaches for Multidrug-Resistant Superbugs Linked to Neurological Anomalies.Pharmaceutics · 2022Review
- Akt Inhibition Promotes Autophagy and Clearance of Group BPathogens (Basel, Switzerland) · 2022Article
- The group AInfectious microbes & diseases · 2022Article
- Review
- Group BPathogens (Basel, Switzerland) · 2022Article
- Case report: Cryptogenic giant brain abscess caused byFrontiers in neurology · 2022Article
- Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5).Autophagy · 2021Article
- Functional Insights into the High-Molecular-Mass Penicillin-Binding Proteins of Streptococcus agalactiae Revealed by Gene Deletion and Transposon Mutagenesis Analysis.Journal of bacteriology · 2021Article
- Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption.Virulence · 2020Article
- Genetic Basis Underlying the Hyperhemolytic Phenotype of Streptococcus agalactiae Strain CNCTC10/84.Journal of bacteriology · 2020Article
- Genome-Wide Assessment of Streptococcus agalactiae Genes Required for Survival in Human Whole Blood and Plasma.Infection and immunity · 2020Article
- Article
- Nicotine Reduces Human Brain Microvascular Endothelial Cell Response toFrontiers in cellular and infection microbiology · 2020Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Bacterial meningitis occurs when bloodborne pathogens invade and penetrate the blood-brain barrier (BBB), provoking inflammation and disease. Group B Streptococcus (GBS), the leading cause of neonatal meningitis, can enter human brain microvascular endothelial cells (hBMECs), but the host response to intracellular GBS has not been characterized. Here we sought to determine whether antibacterial autophagy, which involves selective recognition of intracellular organisms and their targeting to autophagosomes for degradation, is activated in BBB endothelium during bacterial infection. GBS infection resulted in increased punctate distribution of GFP-microtubule-associated protein 1 light chain 3 (LC3) and increased levels of endogenous LC3-II and p62 turnover, two hallmark indicators of active autophagic flux. Infection with GBS mutants revealed that bacterial invasion and the GBS pore-forming β-hemolysin/cytolysin (β-h/c) trigger autophagic activation. Cell-free bacterial extracts containing β-h/c activity induced LC3-II conversion, identifying this toxin as a principal provocative factor for autophagy activation. These results were confirmed in vivo using a mouse model of GBS meningitis as infection with WT GBS induced autophagy in brain tissue more frequently than a β-h/c-deficient mutant. Elimination of autophagy using Atg5-deficient fibroblasts or siRNA-mediated impairment of autophagy in hBMECs led to increased recovery of intracellular GBS. However, electron microscopy revealed that GBS was rarely found within double membrane autophagic structures even though we observed GBS-LC3 co-localization. These results suggest that although autophagy may act as a BBB cellular defense mechanism in response to invading and toxin-producing bacteria, GBS may actively thwart the autophagic pathway.
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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.