Evidence map›Paper›PMID 26873648›Full record

ArticleJournal of autoimmunity2016

Intestinal CCL25 expression is increased in colitis and correlates with inflammatory activity.

Palak J Trivedi, Tony Bruns, Stephen Ward, Martina Mai, Carsten Schmidt, Gideon M Hirschfield, Chris J Weston, David H Adams

Open access · hybridAbstract read
In one paragraph

Article in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
7.8field-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

56 citing papers in PubMed, 90 citations in OpenAlex.

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  7. Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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 3 institutions in 2 countries.

Palak J TrivediNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom; Liver Unit, Queen Elizabeth Hospital, Birmingham, United Kingdom.
Tony BrunsNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom; Dept. of Internal Medicine IV, University Hospital Jena, Jena, Germany; Center for Sepsis Control and Care, University Hospital Jena, Jena, Germany.
Stephen WardNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom; Department of General and Colorectal Surgery, Queen Elizabeth Hospital, Birmingham, United Kingdom.
Martina MaiDept. of Internal Medicine IV, University Hospital Jena, Jena, Germany; Center for Sepsis Control and Care, University Hospital Jena, Jena, Germany.
Carsten SchmidtDept. of Internal Medicine IV, University Hospital Jena, Jena, Germany.
Gideon M HirschfieldNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom; Liver Unit, Queen Elizabeth Hospital, Birmingham, United Kingdom.
Chris J WestonNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom.
David H AdamsNational Institute for Health Research (NIHR) Birmingham Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, University of Birmingham, United Kingdom; Liver Unit, Queen Elizabeth Hospital, Birmingham, United Kingdom. Electronic address: D.H.Adams@bham.ac.uk.
University of Birmingham · GBJena University Hospital · DEQueen Elizabeth Hospital Birmingham · GB

Funding

Wellcome Trust 099907/Z/12/Z
6 · The paper itself

Abstract

CCL25-mediated activation of CCR9 is critical for mucosal lymphocyte recruitment to the intestine. In immune-mediated liver injury complicating inflammatory bowel disease, intrahepatic activation of this pathway allows mucosal lymphocytes to be recruited to the liver, driving hepatobiliary destruction in primary sclerosing cholangitis (PSC). However, in mice and healthy humans CCL25 expression is restricted to the small bowel, whereas few data exist on activation of this pathway in the inflamed colon despite the vast majority of PSC patients having ulcerative colitis. Herein, we show that colonic CCL25 expression is not only upregulated in patients with active colitis, but strongly correlates with endoscopic Mayo score and mucosal TNFα expression. Moreover, approximately 90% (CD4(+)) and 30% (CD8(+)) of tissue-infiltrating T-cells in colitis were identified as CCR9(+) effector lymphocytes, compared to <10% of T-cells being CCR9(+) in normal colon. Sorted CCR9(+) lymphocytes also demonstrated enhanced cellular adhesion to stimulated hepatic sinusoidal endothelium compared with their CCR9(-) counterparts when under flow. Collectively, these results suggest that CCR9/CCL25 interactions are not only involved in colitis pathogenesis but also correlate with colonic inflammatory burden; further supporting the existence of overlapping mucosal lymphocyte recruitment pathways between the inflamed colon and liver.

Indexed as

Gene ExpressionAdultCell AdhesionChemokines, CCColitisColonFemaleGene Expression RegulationHumansInflammatory Bowel DiseasesMaleMiddle AgedReceptors, CCRT-LymphocytesT-Lymphocyte SubsetsTransendothelial and Transepithelial MigrationCC chemokine receptor 9CCL25 protein, humanChemokines, CCReceptors, CCRImmune-mediated liver diseaseInflammatory bowel diseaseLymphocyte recruitmentMucosal immunityPrimary sclerosing cholangitis

Identifiers

PMID26873648
PMCPMC4803021
OpenAlexW2256597409

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.