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Related Concept Videos

The Blood-brain Barrier00:49

The Blood-brain Barrier

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Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
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Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
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Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

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Group B Streptococcus transcriptome when interacting with brain endothelial cells.

Nadine Vollmuth1, Bailey E Bridgers1, Madelyn L Armstrong1

  • 1Department of Biological Sciences, University of Alabama, Tuscaloosa, Alabama, USA.

Journal of Bacteriology
|May 21, 2024
PubMed
Summary
This summary is machine-generated.

Group B Streptococcus (GBS) meningitis is a leading cause of neonatal meningitis. RNA-seq analysis identified GBS virulence factors, with a key regulator, codY, being downregulated, leading to increased bacterial adherence and invasion of brain endothelial cells.

Keywords:
Group B StreptococcusStreptococcus agalactiaeblood–brain barrierbrain endothelial cellstranscriptome

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Area of Science:

  • Microbiology
  • Neuroscience
  • Genetics

Background:

  • Group B Streptococcus (GBS) is the primary cause of bacterial meningitis in newborns.
  • GBS invades the central nervous system by crossing the blood-brain barrier (BBB) and meningeal-cerebrospinal fluid barrier (mBCSFB).
  • Previous GBS virulence factor identification relied on genetic screening.

Purpose of the Study:

  • To identify GBS virulence-associated genes using RNA-sequencing (RNA-seq) during interaction with brain endothelial cells (BECs).
  • To investigate the role of downregulated genes, specifically codY, in GBS pathogenesis.
  • To provide transcriptomic data and validated findings for future GBS-BBB interaction research.

Main Methods:

  • RNA-sequencing (RNA-seq) of GBS co-cultured with induced pluripotent stem cell-derived BECs (iBECs).
  • Quantitative PCR (qPCR) to validate RNA-seq findings for codY expression.
  • Generation and phenotypic analysis of GBS codY mutants in two in vitro BEC models.

Main Results:

  • Out of 2,068 GBS genes, 430 showed differential expression upon BEC interaction, with most (360) downregulated.
  • The transcriptional repressor codY was significantly downregulated during GBS-BEC interaction.
  • GBS mutants lacking codY exhibited increased adherence and invasion capabilities in BEC models.

Conclusions:

  • RNA-seq is a valuable tool for identifying GBS virulence modulators during BEC interaction.
  • Downregulation of codY is a key event in GBS pathogenesis, enhancing bacterial BBB traversal.
  • This study provides a validated transcriptomic dataset offering insights into GBS-BBB interaction pathways.