Evidence map›Paper›PMID 19103772›Full record

ArticleInfection and immunity2009

Defects in innate immunity predispose C57BL/6J-Leprdb/Leprdb mice to infection by Staphylococcus aureus.

Sunny Park, Jeremy Rich, Frank Hanses, Jean C Lee

Abstract read
In one paragraph

Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Frontiers in microbiology · 2025
    Article
  3. Review
  4. Dynamic Adhesive Behavior and Biofilm Formation ofMaterials (Basel, Switzerland) · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Bacteriophage therapy as an alternative technique for treatment of multidrug-resistant bacteria causing diabetic foot infection.International microbiology : the official journal of the Spanish Society for Microbiology · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

1 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

4 authors at 1 institution in 1 country.

Sunny ParkDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Channing Laboratory, Boston, MA 02115, USA.
Jeremy Rich
Frank Hanses
Jean C Lee
Harvard University · US

Funding

INFECTIOUS DISEASE AND BASIC MICROBIOLOGICAL MECHANISMST32AI007061 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 1985 to 2026
$12.1M
GENETIC ANALYSIS OF S AUREUS CAPSULE PRODUCTIONR01AI029040 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, JEAN CLAIRE · 1990 to 2005
$1.5M
GENETIC ANALYSIS OF S. AUREUS CAPSULE PRODUCTIONR21AI029040 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, JEAN CLAIRE · 2000 to 2000
$285k
NIAID NIH HHS AI29040NIAID NIH HHS R01 AI029040NIAID NIH HHS R21 AI029040NIAID NIH HHS T32 AI007061NIAID NIH HHS T32 AI07061
6 · The paper itself

Abstract

Foot and ankle infections are the most common cause of hospitalization among diabetic patients, and Staphylococcus aureus is a major pathogen implicated in these infections. Patients with insulin-resistant (type 2) diabetes are more susceptible to bacterial infections than nondiabetic subjects, but the pathogenesis of these infections is poorly understood. C57BL/6J-Lepr(db)/Lepr(db) (hereafter, db/db) mice develop type 2 diabetes due to a recessive, autosomal mutation in the leptin receptor. We established a S. aureus hind paw infection in diabetic db/db and nondiabetic Lepr(+/+) (+/+) mice to investigate host factors that predispose diabetic mice to infection. Nondiabetic +/+ mice resolved the S. aureus hind paw infection within 10 days, whereas db/db mice with persistent hyperglycemia developed a chronic infection associated with a high bacterial burden. Diabetic db/db mice showed a more robust neutrophil infiltration to the infection site and higher levels of chemokines in the infected tissue than +/+ mice. Blood from +/+ mice killed S. aureus in vitro, whereas db/db blood was defective in bacterial killing. Compared with peripheral blood neutrophils from +/+ mice, db/db neutrophils demonstrated a diminished respiratory burst when stimulated with S. aureus. However, bone marrow-derived neutrophils from +/+ and db/db mice showed comparable phagocytosis and bactericidal activity. Our results indicate that diabetic db/db mice are more susceptible to staphylococcal infection than their nondiabetic littermates and that persistent hyperglycemia modulates innate immunity in the diabetic host.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Immunity, InnateMaleMiceMice, Inbred C57BLMice, Mutant StrainsNeutrophilsReceptors, LeptinStaphylococcal Skin InfectionsStaphylococcus aureusReceptors, Leptin

Identifiers

PMID19103772
PMCPMC2643648
OpenAlexW2108246274

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.