Evidence map›Paper›PMID 18981162›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Intestinal macrophage/epithelial cell-derived CCL11/eotaxin-1 mediates eosinophil recruitment and function in pediatric ulcerative colitis.

Richard Ahrens, Amanda Waddell, Luqman Seidu, Carine Blanchard, Rebecca Carey, Elizabeth Forbes, Maria Lampinen, Tara Wilson, Elizabeth Cohen, Keith Stringer and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 3% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
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  7. Article
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  11. Review
  12. Article
  13. Article
  14. Eosinophils: old cells, new directions.Frontiers in medicine · 2024
    Review
  15. Macrophage Migration Inhibitory Factor inInternational journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

41 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

18 authors at 4 institutions in 3 countries.

Richard AhrensDivision of Allergy and Immunology, Department of Pediatrics, University of Cincinnati College of Medicine, CCHMC, Cincinnati, OH 45229, USA.
Amanda Waddell
Luqman Seidu
Carine Blanchard
Rebecca Carey
Elizabeth Forbes
Maria Lampinen
Tara Wilson
Elizabeth Cohen
Keith Stringer
Edgar Ballard
Ariel Munitz
Huan Xu
Nancy Lee
James J Lee
Marc E Rothenberg
Lee Denson
Simon P Hogan
National Institute of Allergy and Infectious Diseases · USMayo Clinic in Arizona · USCincinnati Children's Hospital Medical Center · USUppsala University · SE

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Kathryn Ann Wikenheiser-Brokamp · 2007 to 2026
$24.4M
Growth Hormone Receptor Dimerization/Disulfide LinkageR01DK058259 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FRANK, STUART J · 2001 to 2014
$3.4M
Cytokine Regulation of Growth Hormone SignalingR01DK068164 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI DENSON, LEE ARMISTEAD · 2006 to 2010
$1.4M
NIDDK NIH HHS 1P30DK078392-01NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK058259NIDDK NIH HHS R01 DK068164
6 · The paper itself

Abstract

Clinical studies have demonstrated a link between the eosinophil-selective chemokines, eotaxins (eotaxin-1/CCL11 and eotaxin-2/CCL24), eosinophils, and the inflammatory bowel diseases, Crohn's disease and ulcerative colitis (UC). However, the cellular source and individual contribution of the eotaxins to colonic eosinophilic accumulation in inflammatory bowel diseases remain unclear. In this study we demonstrate, by gene array and quantitative PCR, elevated levels of eotaxin-1 mRNA in the rectosigmoid colon of pediatric UC patients. We show that elevated levels of eotaxin-1 mRNA positively correlated with rectosigmoid eosinophil numbers. Further, colonic eosinophils appeared to be degranulating, and the levels positively correlated with disease severity. Using the dextran sodium sulfate (DSS)-induced intestinal epithelial injury model, we show that DSS treatment of mice strongly induced colonic eotaxin-1 and eotaxin-2 expression and eosinophil levels. Analysis of eosinophil-deficient mice defined an effector role for eosinophils in disease pathology. DSS treatment of eotaxin-2(-/-) and eotaxin-1/2(-/-) mice demonstrated that eosinophil recruitment was dependent on eotaxin-1. In situ and immunofluorescence analysis-identified eotaxin-1 expression was restricted to intestinal F4/80(+)CD11b(+) macrophages in DSS-induced epithelial injury and to CD68(+) intestinal macrophages and the basolateral compartment of intestinal epithelial cells in pediatric UC. These data demonstrate that intestinal macrophage and epithelial cell-derived eotaxin-1 plays a critical role in the regulation of eosinophil recruitment in colonic eosinophilic disease such as pediatric UC and provides a basis for targeting the eosinophil/eotaxin-1 axis in UC.

Indexed as

AdolescentAnimalsChemokine CCL11Chemotaxis, LeukocyteChildChild, PreschoolColitis, UlcerativeColonEosinophilsEpithelial CellsFemaleFlow CytometryFluorescent Antibody TechniqueHumansImmunohistochemistryIntestinal MucosaChemokine CCL11RNA, Messenger

Identifiers

PMID18981162
PMCPMC2728352
OpenAlexW1652381613

What OpenQuestion holds

Textmetadata
LicenceTDM
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.