ArticleCellular microbiology2010
Activation of brain endothelium by pneumococcal neuraminidase NanA promotes bacterial internalization.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 78 citations in OpenAlex.
- Stem cell-derived brain-like endothelial cells to interrogateVirulence · 2025Article
- Molecular mechanisms of streptococcal disruption of the blood-brain barrier and their pathogenic role in bacterial meningitis.Frontiers in immunology · 2025Review
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- Co-infection of the respiratory epithelium, scene of complex functional interactions between viral, bacterial, and human neuraminidases.Frontiers in microbiology · 2023Review
- Review
- Cytokine response in cerebrospinal fluid of meningitis patients and outcome associated with pneumococcal serotype.Scientific reports · 2021Article
- Transcriptomic analysis of human brain microvascular endothelial cells exposed to laminin binding protein (adhesion lipoprotein) and Streptococcus pneumoniae.Scientific reports · 2021Article
- Pneumococcal Encounter With the Blood-Brain Barrier Endothelium.Frontiers in cellular and infection microbiology · 2020Review
- In vivo proteomics identifies the competence regulon and AliB oligopeptide transporter as pathogenic factors in pneumococcal meningitis.PLoS pathogens · 2019Article
- In silico analysis as a strategy to identify candidate epitopes with human IgG reactivity to study Porphyromonas gingivalis virulence factors.AMB Express · 2019Article
- Review
- Activation of brain endothelium by Escherichia coli K1 virulence factor cglD promotes polymorphonuclear leukocyte transendothelial migration.Medical microbiology and immunology · 2019Article
- Past and Current Perspectives in Modeling Bacteria and Blood-Brain Barrier Interactions.Frontiers in microbiology · 2019Article
- Sialidases FromFrontiers in cellular and infection microbiology · 2019Review
- Mechanisms of Blood Brain Barrier Disruption by Different Types of Bacteria, and Bacterial-Host Interactions Facilitate the Bacterial Pathogen Invading the Brain.Cellular and molecular neurobiology · 2018Review
- Characterization of a Two-Component System Transcriptional Regulator, LtdR, That Impacts Group B Streptococcal Colonization and Disease.Infection and immunity · 2018Article
- Proteomic and bioinformatic pipeline to screen the ligands of S. pneumoniae interacting with human brain microvascular endothelial cells.Scientific reports · 2018Article
- Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis.Virulence · 2018Article
- Zinc metalloproteinase ZmpC suppresses experimental pneumococcal meningitis by inhibiting bacterial invasion of central nervous systems.Virulence · 2017Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Streptococcus pneumoniae (SPN), the leading cause of meningitis in children and adults worldwide, is associated with an overwhelming host inflammatory response and subsequent brain injury. Here we examine the global response of the blood-brain barrier to SPN infection and the role of neuraminidase A (NanA), an SPN surface anchored protein recently described to promote central nervous system tropism. Microarray analysis of human brain microvascular endothelial cells (hBMEC) during infection with SPN or an isogenic NanA-deficient (ΔnanA) mutant revealed differentially activated genes, including neutrophil chemoattractants IL-8, CXCL-1, CXCL-2. Studies using bacterial mutants, purified recombinant NanA proteins and in vivo neutrophil chemotaxis assays indicated that pneumococcal NanA is necessary and sufficient to activate host chemokine expression and neutrophil recruitment during infection. Chemokine induction was mapped to the NanA N-terminal lectin-binding domain with a limited contribution of the sialidase catalytic activity, and was not dependent on the invasive capability of the organism. Furthermore, pretreatment of hBMEC with recombinant NanA protein significantly increased bacterial invasion, suggesting that NanA-mediated activation of hBMEC is a prerequisite for efficient SPN invasion. These findings were corroborated in an acute murine infection model where we observed less inflammatory infiltrate and decreased chemokine expression following infection with the ΔnanA mutant.
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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.