ArticlePLoS pathogens2019
A streptococcal Fic domain-containing protein disrupts blood-brain barrier integrity by activating moesin in endothelial cells.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Zoonotic Streptococcus imports glucose to inhibit stringent response and promote growth during meningitis.Nature microbiology · 2026Article
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Endogenous Type I-C CRISPR-Cas system ofFrontiers in microbiology · 2024Article
- A novel aquaporin Aagp contributes toVirulence · 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
- Outbreak of PathogenicPathogens (Basel, Switzerland) · 2023Article
- Blood-Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets.International journal of molecular sciences · 2023Review
- BifA Triggers Phosphorylation of Ezrin to BenefitBiomedicines · 2022Article
- Moesin Is a Novel Biomarker of Endothelial Injury in Sepsis.Journal of immunology research · 2021Article
- This was the year that was: brain barriers and brain fluid research in 2019.Fluids and barriers of the CNS · 2020Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Streptococcus equi subsp. zooepidemicus (SEZ) is a zoonotic pathogen capable of causing meningitis in humans. The mechanisms that enable pathogens to traverse the blood-brain barrier (BBB) are incompletely understood. Here, we investigated the role of a newly identified Fic domain-containing protein, BifA, in SEZ virulence. BifA was required for SEZ to cross the BBB and to cause meningitis in mice. BifA also enhanced SEZ translocation across human Brain Microvascular Endothelial Cell (hBMEC) monolayers. Purified BifA or its Fic domain-containing C-terminus alone were able to enter into hBMECs, leading to disruption of monolayer barrier integrity. A SILAC-based proteomic screen revealed that BifA binds moesin. BifA's Fic domain was required for its binding to this regulator of host cell cytoskeletal processes. BifA treatment of hBMECs led to moesin phosphorylation and downstream RhoA activation. Inhibition of moesin activation or moesin depletion in hBMEC monolayers abrogated BifA-mediated increases in barrier permeability and SEZ's capacity to translocate across monolayers. Thus, BifA activation of moesin appears to constitute a key mechanism by which SEZ disrupts endothelial monolayer integrity to penetrate the BBB.
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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.