Evidence map›Paper›PMID 17255321›Full record

ArticleThe American journal of pathology2007

CXCL1/KC and CXCL2/MIP-2 are critical effectors and potential targets for therapy of Escherichia coli O157:H7-associated renal inflammation.

James K Roche, Tiffany R Keepers, Lisa K Gross, Regina M Seaner, Tom G Obrig

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.6field-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

39 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. The immune mechanisms of the urinary tract against infections.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Article
  6. Article
  7. CommensalAnimals : an open access journal from MDPI · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Verotoxin Receptor-Based Pathology and Therapies.Frontiers in cellular and infection microbiology · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. SIRT2 Regulates LPS-Induced Renal Tubular CXCL2 and CCL2 Expression.Journal of the American Society of Nephrology : JASN · 2015
    Article
  20. Article
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

5 authors at 1 institution in 1 country.

James K RocheDivision of Nephrology, Department of Medicine, Box 800133, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.
Tiffany R Keepers
Lisa K Gross
Regina M Seaner
Tom G Obrig
University of Virginia · US

Funding

Vaccine strategy for broad spectrum protection agains non-typhoidal salmonellU54AI057168 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BUSHMAN, FREDERIC D · 2003 to 2013
$91.5M
SHIGA TOXIN MODE OF ACTION IN BACTERIAL DISEASESR01AI024431 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OBRIG, TOM G · 1989 to 2007
$2.9M
NEW THERAPEUTICS FOR PATHOGENIC E-COLI DISEASESU01AI054782 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OBRIG, TOM G · 2003 to 2007
$2.8M
NIAID NIH HHS R01 AI024431NIAID NIH HHS U01 AI054782NIAID NIH HHS U54 AI057168
6 · The paper itself

Abstract

Neutrophilia is a characteristic of hemolytic uremic syndrome caused by Shiga toxin (Stx2)-producing Escherichia coli. However, the role of neutrophils in the toxin-induced renal injury occurring in enterohemorrhagic E. coli infection remains undefined. We report the trafficking of neutrophils to the kidney of C57BL/6 mice throughout a 72-hour time course after challenge with purified E. coli Stx2 and lipopolysaccharide (LPS). Increased neutrophils were observed in the renal cortex, particularly within the glomeruli where a more than fourfold increase in neutrophils was noted within 2 hours after challenge. Using microarray analysis, an increased number of transcripts for chemoattractants CXCL1/KC (69-fold at 2 hours) and CXCL2/MIP-2 (29-fold at 2 hours) were detected. Ribonuclease protection assays, Northern blotting, enzyme-linked immunosorbent assay, and immunohistochemistry confirmed microarray results, showing that both chemokines were expressed only on the immediate periglomerular epithelium and that these events coincided with neutrophil invasion of glomeruli. Co-administration of Stx2 with LPS enhanced and prolonged the KC and MIP-2 host response (RNA and protein) induced by LPS alone. Immunoneutralization in vivo of CXCL1/KC and CXCL2/MIP-2 abrogated neutrophil migration into glomeruli by 85%. These data define the molecular basis for neutrophil migration into the kidney after exposure to virulence factors of Shiga toxin-producing E. coli O157:H7.

Indexed as

Escherichia coli O157AnimalsCell MovementChemokine CXCL1Chemokine CXCL2ChemokinesChemokines, CXCEscherichia coli InfectionsInflammationKidney GlomerulusLipopolysaccharidesMaleMiceNephritisNeutrophil InfiltrationNeutrophilsChemokine CXCL1Chemokine CXCL2ChemokinesChemokines, CXCCxcl1 protein, mouseCxcl2 protein, mouseLipopolysaccharidesShiga Toxin 2

Identifiers

PMID17255321
PMCPMC1851848
OpenAlexW2091057162

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.