Evidence map›Paper›PMID 16177366›Full record

ArticleInfection and immunity2005

Poly-N-acetylglucosamine production in Staphylococcus aureus is essential for virulence in murine models of systemic infection.

Andrea Kropec, Tomas Maira-Litran, Kimberly K Jefferson, Martha Grout, Sarah E Cramton, Friedrich Götz, Donald A Goldmann, Gerald B Pier

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

92 citing papers in PubMed, 161 citations in OpenAlex.

  1. ImagingmBio · 2026
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  7. Poly-Frontiers in microbiology · 2024
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  16. The Role ofAntibiotics (Basel, Switzerland) · 2021
    Review
  17. Within-Host Adaptation ofInternational journal of molecular sciences · 2021
    Article
  18. A Narrative Review on the Role ofOpen forum infectious diseases · 2021
    Review
  19. Article
  20. Plasmid-Chromosome Crosstalk inFrontiers in cellular and infection microbiology · 2021
    Article

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Andrea KropecChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Tomas Maira-Litran
Kimberly K Jefferson
Martha Grout
Sarah E Cramton
Friedrich Götz
Donald A Goldmann
Gerald B Pier
Harvard University · USUniversity of Tübingen · DEBoston Children's Hospital · USBrigham and Women's Hospital · USUniversity Medical Center Freiburg · DE

Funding

Virulence and Immunity to StaphylcocciR01AI046706 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 2001 to 2010
$4.1M
VIRULENCE AND IMMUNITY TO STAPHYLOCOCCIR21AI046706 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 2000 to 2000
$418k
Antibiotic resistance of S. aureus biofilmsR21AI061590 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI JEFFERSON, KIMBERLY KAY · 2004 to 2005
$402k
NIAID NIH HHS AI061590NIAID NIH HHS AI46706NIAID NIH HHS R01 AI046706NIAID NIH HHS R21 AI046706NIAID NIH HHS R21 AI061590
6 · The paper itself

Abstract

The contribution of the Staphylococcus aureus surface polysaccharide poly-N-acetylglucosamine (PNAG) to virulence was evaluated in three mouse models of systemic infection: bacteremia, renal abscess formation, and lethality following high-dose intraperitoneal (i.p.) infection. Deletion of the intercellular adhesin (ica) locus that encodes the biosynthetic enzymes for PNAG production in S. aureus strains Mn8, Newman, and NCTC 10833 resulted in mutant strains with significantly reduced abilities to maintain bacterial levels in blood following intravenous or i.p. injection, to spread systemically to the kidneys following i.p. injection, or to induce a moribund/lethal state following i.p. infection. In the bacteremia model, neither growth phase nor growth medium used to prepare the S. aureus inoculum affected the conclusion that PNAG production was needed for full virulence. As the SarA regulatory protein has been shown to affect ica transcription, PNAG synthesis, and biofilm formation, we also evaluated S. aureus strains Mn8 and 10833 deleted for the sarA gene in the renal infection model. A decrease in PNAG production was seen in sarA mutants using immunoblots of cell surface extracts but was insufficient to reduce the virulence of sarA-deleted strains in this model. S. aureus strains deleted for the ica genes were much more susceptible to antibody-independent opsonic killing involving human peripheral blood leukocytes and rabbit complement. Thus, PNAG confers on S. aureus resistance to killing mediated by these innate host immune mediators. Overall, PNAG production by S. aureus appears to be a critical virulence factor as assessed in murine models of systemic infection.

Indexed as

Adhesins, BacterialAnimalsBacteremiaBacterial Proteinsbeta-GlucansDisease Models, AnimalGene DeletionImmunity, InnateMicePhagocytosisStaphylococcal InfectionsStaphylococcus aureusVirulenceAdhesins, Bacterialadhesin, Staphylococcus aureusBacterial Proteinsbeta-Glucanspoly-N-acetyl-1-6-glucosamineSarA protein, Staphylococcus aureus

Identifiers

PMID16177366
PMCPMC1230935
OpenAlexW2104283571

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.