Evidence map›Paper›PMID 16138192›Full record

ArticleThe Journal of clinical investigation2005

Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid.

Kelly S Doran, Erin J Engelson, Arya Khosravi, Heather C Maisey, Iris Fedtke, Ozlem Equils, Kathrin S Michelsen, Moshe Arditi, Andreas Peschel, Victor Nizet

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
9.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

140 citing papers in PubMed, 236 citations in OpenAlex.

  1. Article
  2. A cross-strain CRISPRi sgRNA library forMicrobiology resource announcements · 2026
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  3. Pathogens (Basel, Switzerland) · 2026
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  4. CRISPR interference in aJournal of bacteriology · 2026
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  5. Article
  6. Article
  7. Article
  8. Identification of glyoxalase A in group BInfection and immunity · 2025
    Article
  9. Review
  10. Article
  11. Mechanisms and Manifestations of Group B Streptococcus Meningitis in Newborns.Journal of the Pediatric Infectious Diseases Society · 2025
    Review
  12. Article
  13. Article
  14. Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024
    Article
  15. Microbiology resource announcements · 2024
    Article
  16. Article
  17. Re-framing the importance of Group BInfection and immunity · 2024
    Review
  18. Group BJournal of bacteriology · 2024
    Article
  19. Science advances · 2024
    Article
  20. iScience · 2024
    Article

80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Kelly S DoranDepartment of Pediatrics, Division of Infectious Diseases, UCSD School of Medicine, La Jolla, California 92093, USA. kdoran@ucsd.edu
Erin J Engelson
Arya Khosravi
Heather C Maisey
Iris Fedtke
Ozlem Equils
Kathrin S Michelsen
Moshe Arditi
Andreas Peschel
Victor Nizet
Cedars-Sinai Medical Center · USUniversity of California, San Diego · USUniversity of Tübingen · DEWageningen University & Research · NL

Funding

PENETRATION OF THE BLOOD BRAIN BARRIER IN GBS MENINGITISR03HD037224 · NICHD · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI NIZET, VICTOR · 1999 to 2000
$76k
NICHD NIH HHS HD-37224
6 · The paper itself

Abstract

Group B streptococci (GBSs) are the leading cause of neonatal meningitis. GBSs enter the CNS by penetrating the blood-brain barrier (BBB), which consists of specialized human brain microvascular endothelial cells (hBMECs). To identify GBS factors required for BBB penetration, we generated random mutant libraries of a virulent strain and screened for loss of hBMEC invasion in vitro. Two independent hypo-invasive mutants possessed disruptions in the same gene, invasion associated gene (iagA), which encodes a glycosyltransferase homolog. Allelic replacement of iagA in the GBS chromosome produced a 4-fold decrease in hBMEC invasiveness. Mice challenged with the GBS DeltaiagA mutant developed bacteremia comparably to WT mice, yet mortality was significantly lower (20% vs. 90%), as was the incidence of meningitis. The glycolipid diglucosyldiacylglycerol, a cell membrane anchor for lipoteichoic acid (LTA) and predicted product of the IagA glycosyltransferase, was absent in the DeltaiagA mutant, which consequently shed LTA into the media. Attenuation of virulence of the DeltaiagA mutant was found to be independent of TLR2-mediated signaling, but bacterial supernatants from the DeltaiagA mutant containing released LTA inhibited hBMEC invasion by WT GBS. Our data suggest that LTA expression on the GBS surface plays a role in bacterial interaction with BBB endothelium and the pathogenesis of neonatal meningitis.

Indexed as

AnimalsBiological TransportBlood-Brain BarrierBrainCell MembraneEndothelial CellsEndothelium, VascularGlycolipidsHumansInfant, NewbornLipopolysaccharidesMeningitis, BacterialMiceMice, Inbred C57BLStreptococcus agalactiaeTeichoic AcidsGlycolipidsLipopolysaccharideslipoteichoic acidTeichoic Acids

Identifiers

PMID16138192
PMCPMC1193870
OpenAlexW2127690345

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.