ArticleThe Journal of clinical investigation2015
Bacterial induction of Snail1 contributes to blood-brain barrier disruption.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Bacterial extracellular vesicles - brain invaders? A systematic review.Frontiers in molecular neuroscience · 2023Pooled it
- Article
- Rapamycin Prevents Sulfate-Reducing Bacteria-Induced Effects on Snail and GSK-3 and Impaired Intestinal Barrier.Microorganisms · 2026Article
- A new chromosome-level genome assembly for western painted turtle Chrysemys picta bellii, a model for extreme physiological adaptations.BMC genomics · 2026Article
- Tau is necessary for Pseudomonas aeruginosa-induced blood-brain barrier dysfunction.Communications biology · 2026Article
- Gardenoside restores blood-brain barrier integrity following ischemic stroke via AMPK-dependent ZO-1 preservation.Frontiers in behavioral neuroscience · 2026Article
- Stem cell-derived brain-like endothelial cells to interrogateVirulence · 2025Article
- Article
- Group B Streptococci lyse endothelial cells to infect the brain in a zebrafish meningitis model.PLoS biology · 2025Article
- In Vitro Comparison of Two Python-Based Programs for the Automated Analysis of Tight-Junction Phenotype in Brain Endothelium During Bacterial Infection.Cell biochemistry and function · 2025Article
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Identification of glyoxalase A in group BInfection and immunity · 2025Article
- Sulfate reducing bacteria induce α-synuclein in intestinal and neuronal cells and tissues and inhibit tyrosine hydroxylase in neuronal cells.Frontiers in neuroscience · 2025Article
- Time-course transcriptomics reveals the impact ofFrontiers in microbiology · 2025Article
- Molecular mechanisms of streptococcal disruption of the blood-brain barrier and their pathogenic role in bacterial meningitis.Frontiers in immunology · 2025Review
- Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024Article
- Article
- Article
- Common Chemical Plasticizer Di(2-Ethhylhexyl) Phthalate Exposure Exacerbates Coxsackievirus B3 Infection.Viruses · 2024Article
- The hypervirulent Group B Streptococcus HvgA adhesin promotes central nervous system invasion through transcellular crossing of the choroid plexus.Fluids and barriers of the CNS · 2024Article
28 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
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Bacterial meningitis is a serious infection of the CNS that results when blood-borne bacteria are able to cross the blood-brain barrier (BBB). Group B Streptococcus (GBS) is the leading cause of neonatal meningitis; however, the molecular mechanisms that regulate bacterial BBB disruption and penetration are not well understood. Here, we found that infection of human brain microvascular endothelial cells (hBMECs) with GBS and other meningeal pathogens results in the induction of host transcriptional repressor Snail1, which impedes expression of tight junction genes. Moreover, GBS infection also induced Snail1 expression in murine and zebrafish models. Tight junction components ZO-1, claudin 5, and occludin were decreased at both the transcript and protein levels in hBMECs following GBS infection, and this repression was dependent on Snail1 induction. Bacteria-independent Snail1 expression was sufficient to facilitate tight junction disruption, promoting BBB permeability to allow bacterial passage. GBS induction of Snail1 expression was dependent on the ERK1/2/MAPK signaling cascade and bacterial cell wall components. Finally, overexpression of a dominant-negative Snail1 homolog in zebrafish elevated transcription of tight junction protein-encoding genes and increased zebrafish survival in response to GBS challenge. Taken together, our data support a Snail1-dependent mechanism of BBB disruption and penetration by meningeal pathogens.
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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.