Evidence map›Paper›PMID 18974303›Full record

ArticleThe American journal of pathology2008

Immunological mechanisms underlying the genetic predisposition to severe Staphylococcus aureus infection in the mouse model.

Maren von Köckritz-Blickwede, Manfred Rohde, Sonja Oehmcke, Lloyd S Miller, Ambrose L Cheung, Heiko Herwald, Simon Foster, Eva Medina

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Role and plasticity of Th1 and Th17 responses in immunity toHuman vaccines & immunotherapeutics · 2019
    Trial
  3. GrowingInfection and immunity · 2026
    Article
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Frontiers in cellular and infection microbiology · 2024
    Article
  14. Article
  15. Article
  16. iScience · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Article

25 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 5 countries.

Maren von Köckritz-BlickwedeResearch Group Infection Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Manfred Rohde
Sonja Oehmcke
Lloyd S Miller
Ambrose L Cheung
Heiko Herwald
Simon Foster
Eva Medina
Helmholtz Centre for Infection Research · DELaboratory of Molecular Genetics · PLDartmouth College · USUniversity of California, Los Angeles · USUniversity of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Host genetic variations play a significant role in conferring predisposition to infection. In this study, we examined the immune mechanisms underlying the host genetic predisposition to severe Staphylococcus aureus infection in different mouse strains. Whereas C57BL/6 mice were the most resistant in terms of control of bacterial growth and survival, A/J, DBA/2, and BALB/c mice were highly susceptible and succumbed to infection shortly after bacterial inoculation. Other strains (C3H/HeN, CBA, and C57BL/10) exhibited intermediate susceptibility levels. Susceptibility of mice to S. aureus was associated with an inability to limit bacterial growth in the kidneys and development of pathology. Resistance to S. aureus in C57BL/6 mice was dependent on innate immune mechanisms because Rag2-IL2Rgamma(-/-) C57BL/6 mice, which are deficient in B, T, and NK cells, were also resistant to infection. Indeed, neutrophil depletion or inhibition of neutrophil recruitment rendered C57BL/6 mice completely susceptible to S. aureus, indicating that neutrophils are essential for the observed resistance. Although neutrophil function is not inhibited in A/J mice, expression of neutrophil chemoattractants KC and MIP-2 peaked earlier in the kidneys of C57BL/6 mice than in A/J mice, indicating that a delay in neutrophil recruitment to the site of infection may underlie the increased susceptibility of A/J mice to S. aureus.

Indexed as

Disease Models, AnimalGenetic Predisposition to DiseaseAnimalsCytokinesDNA-Binding ProteinsImmunity, InnateInterleukin Receptor Common gamma SubunitKidneyLungMiceMice, Inbred StrainsMice, KnockoutNeutrophilsStaphylococcal InfectionsStaphylococcus aureusSurvival RateCytokinesDNA-Binding ProteinsInterleukin Receptor Common gamma SubunitRag2 protein, mouse

Identifiers

PMID18974303
PMCPMC2626378
OpenAlexW2020552766

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.