Evidence map›Paper›PMID 26462859›Full record

ArticleClinical and experimental immunology2016

Differential expression of key regulators of Toll-like receptors in ulcerative colitis and Crohn's disease: a role for Tollip and peroxisome proliferator-activated receptor gamma?

P Fernandes, J MacSharry, T Darby, A Fanning, F Shanahan, A Houston, E Brint

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  6. Cross-national comparison of inflammatory bowel disease burden in China, Japan, the United States, and India: An age-period-cohort analysis of GBD 2021.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2025
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  14. MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
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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

7 authors at 3 institutions in 2 countries.

P FernandesCork Cancer Research Centre, University College Cork, National University of Ireland.
J MacSharryAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
T DarbyDepartment of Pathology, Emory University, Atlanta, GA, USA.
A FanningAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
F ShanahanAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
A HoustonAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
E BrintAlimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
University College Cork · IENational University of Ireland · IEEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune system is currently seen as the probable initiator of events which culminate in the development of inflammatory bowel disease (IBD) with Toll-like receptors (TLRs) known to be involved in this disease process. Many regulators of TLRs have been described, and dysregulation of these may also be important in the pathogenesis of IBD. The aim of this study was to perform a co-ordinated analysis of the expression levels of both key intestinal TLRs and their inhibitory proteins in the same IBD cohorts, both ulcerative colitis (UC) and Crohn's disease (CD), in order to evaluate the potential roles of these proteins in the pathogenesis of IBD. Of the six TLRs (TLRs 1, 2, 4, 5, 6 and 9) examined, only TLR-4 was increased significantly in IBD, specifically in active UC. In contrast, differential alterations in expression of TLR inhibitory proteins were observed. A20 and suppressor of cytokine signalling 1 (SOCS1) were increased only in active UC while interleukin-1 receptor-associated kinase 1 (IRAK-m) and B cell lymphoma 3 protein (Bcl-3) were increased in both active UC and CD. In contrast, expression of both peroxisome proliferator-activated receptor gamma (PPARγ) and Toll interacting protein (Tollip) was decreased in both active and inactive UC and CD and at both mRNA and protein levels. In addition, expression of both PPARγ and A20 expression was increased by stimulation of a colonic epithelial cell line Caco-2 with both TLR ligands and commensal bacterial strains. These data suggest that IBD may be associated with distinctive changes in TLR-4 and TLR inhibitory proteins, implying that alterations in these may contribute to the pathogenesis of IBD.

Indexed as

AdultAgedB-Cell Lymphoma 3 ProteinCaco-2 CellsColitis, UlcerativeColonCrohn DiseaseFemaleHumansInflammatory Bowel DiseasesInterleukin-1 Receptor-Associated KinasesIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiddle AgedPPAR gammaB-Cell Lymphoma 3 ProteinBCL3 protein, humanInterleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsPPAR gammaProto-Oncogene ProteinsRNA, MessengerSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTOLLIP protein, humanToll-Like Receptor 1Toll-Like Receptor 4Toll-Like ReceptorsTranscription Factorsinflammatory bowel diseasePPARγregulationTollipToll-like receptor

Identifiers

PMID26462859
PMCPMC4750602
OpenAlexW2195840745

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.