Evidence map›Paper›PMID 24874458›Full record

ArticleInflammatory bowel diseases2014

CCL25/CCR9 interactions are not essential for colitis development but are required for innate immune cell protection from chronic experimental murine colitis.

Marc-André Wurbel, Severine Le Bras, Mouna Ibourk, Michael Pardo, Maria G McIntire, Dominique Coco, Raif S Geha, Edda Fiebiger, Scott B Snapper

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The Regulatory Function of CCR9Frontiers in immunology · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. 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

9 authors at 3 institutions in 1 country.

Marc-André WurbelDivisions of *Gastroenterology/Nutrition and †Immunology, Boston Children's Hospital; ‡Department of Pediatrics, Harvard Medical School; and §Department of Pathology, Brigham and Women's Hospital & Harvard Medical School, Boston, Massachusetts.
Severine Le Bras
Mouna Ibourk
Michael Pardo
Maria G McIntire
Dominique Coco
Raif S Geha
Edda Fiebiger
Scott B Snapper
Harvard University · USBrigham and Women's Hospital · USBoston Children's Hospital · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
WIP in TCR signaling and actin reorganizationP01HL059561 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI GEHA, RAIF SALIM · 1997 to 2012
$21.8M
The Pathogenesis Of Colitis In A Novel Th2 Model Of IBDR01AI050950 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SNAPPER, SCOTT B · 2002 to 2013
$2.6M
Studies of Fc-epsilon-RI as an antigen presentation structure at mucosal surfacesR01AI075037 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI FIEBIGER, ELISABETH EDDA · 2009 to 2013
$2.0M
Studies on Fc-epsilon-RI as an antigen presentation structure at mucosal surfacesR56AI075037 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI FIEBIGER, ELISABETH EDDA · 2008 to 2008
$423k
Exploring Regulatory T Cell Dysfunction in a Murine Model of ColitisR56AI050950 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SNAPPER, SCOTT B · 2008 to 2008
$336k
NHLBI NIH HHS HL59561NHLBI NIH HHS P01 HL059561NIAID NIH HHS AI075037NIAID NIH HHS AI50950NIAID NIH HHS R01 AI075037NIAID NIH HHS R56 AI075037NIDDK NIH HHS DK034854NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

backgroundThe chemokine CCL25, and its receptor CCR9, constitute a unique chemokine/receptor pair, which regulates trafficking of T lymphocytes to the small intestine under physiological conditions and is an attractive target for small bowel Crohn's disease drug development. We have previously shown that CCL25/CCR9 interactions regulate the recovery from acute dextran sulfate sodium-induced colonic inflammation. In this study, we explored whether these interactions also regulate chronic colitis development in 2 independent murine models of experimental colitis.

methodsHistological flow cytometry and qPCR analyses were performed to evaluate the role of CL25 and CCR9 in chronic colonic inflammation induced by serial exposures to dextran sulfate sodium salts or by adoptive transfer of CD45RB(hi) CD4(+) T cell into lymphopenic mice devoid of CCL25/CCR9 interactions.

resultsChronic dextran sulfate sodium exposure results in exacerbated colitis in mice deficient for either CCR9 or CCL25 when compared with wild-type control mice. Although CCR9-deficient T cells traffic to the colon and induce severe colitis similar to wild-type T cells in the CD45RB transfer model, naive wild-type T cells induce more severe disease in recipient animals devoid of CCL25 expression.

conclusionsCCL25/CCR9 interactions are required for modulating protection against large intestinal inflammation in 2 models of chronic colitis. These data may have implications for the potential effects of disrupting CCL25/CCR9 interactions in humans in the setting of intestinal disorders including inflammatory bowel disease.

Indexed as

AnimalsChemokines, CCChronic DiseaseColitisCytoprotectionDisease Models, AnimalFemaleFlow CytometryImmunity, InnateMaleMiceRandom AllocationReceptors, CCRReference ValuesSensitivity and SpecificityCC chemokine receptor 9Ccl25 protein, mouseChemokines, CCReceptors, CCR

Identifiers

PMID24874458
PMCPMC6249688
OpenAlexW2333308480

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.