Evidence map›Paper›PMID 26536229›Full record

ArticlePloS one2015

Expression of CCL20 and Its Corresponding Receptor CCR6 Is Enhanced in Active Inflammatory Bowel Disease, and TLR3 Mediates CCL20 Expression in Colonic Epithelial Cells.

Helene Kolstad Skovdahl, Atle van Beelen Granlund, Ann Elisabet Østvik, Torunn Bruland, Ingunn Bakke, Sverre Helge Torp, Jan Kristian Damås, Arne Kristian Sandvik

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  3. Colonic epithelial regeneration shapes susceptibility tobioRxiv : the preprint server for biology · 2026
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  7. P2YJournal of immunology research · 2026
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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 2 institutions in 1 country.

Helene Kolstad SkovdahlCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Atle van Beelen GranlundCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Ann Elisabet ØstvikCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Torunn BrulandDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Ingunn BakkeDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Sverre Helge TorpDepartment of Laboratory Medicine, Children and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
Jan Kristian DamåsCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Arne Kristian SandvikCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Norwegian University of Science and Technology · NOSt Olav's University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe chemokine CCL20 and its receptor CCR6 are putative drug targets in inflammatory bowel disease, and CCL20 is a novel IBD predilection gene. Previous findings on the CCL20 response in these diseases are divergent. This study was undertaken to examine CCL20 and CCR6 during active and inactive disease, and mechanisms for CCL20 regulation by the innate immune system. As TLR3 has recently emerged as a possible mediator of CCL20 production, we hypothesised that this TLR plays an important role in enterocytic CCL20 production.

methodsA large microarray study on colonic pinch biopsies from active and inactive ulcerative colitis and Crohn's disease provided background information. CCL20 and CCR6 were localized and their expression levels assessed in biopsies using in situ hybridization and immunohistochemistry. Regulation of CCL20 was studied in the HT29 cell line using a panel of pattern recognition receptor ligands followed by a TLR3 siRNA assay.

resultsCCL20 and CCR6 mRNA abundances were increased during active inflammation (CCL20 5.4-fold in ulcerative colitis and 4.2-fold in Crohn's disease; CCR6 1.8 and 2.0, respectively). CCL20 and CCR6 mRNA positive immune cells in lamina propria were more numerous, and CCL20 immunoreactivity increased massively in the epithelial cells during active inflammation for both diseases. TLR3 stimulation potently induced upregulation and release of CCL20 from HT29 cells, and TLR3 silencing reduced CCL20 mRNA and protein levels.

conclusionsThe CCL20-CCR6 axis is involved during active inflammation in both ulcerative colitis and Crohn's disease. The epithelial cells seem particularly involved in the CCL20 response, and results from this study strongly suggest that the innate immune system is important for activation of the epithelium, especially through TLR3.

Indexed as

AdultAgedCase-Control StudiesCell ProliferationCells, CulturedChemokine CCL20ColonEpithelial CellsFemaleHumansImmunoenzyme TechniquesInflammatory Bowel DiseasesIn Situ HybridizationMaleMiddle AgedReal-Time Polymerase Chain ReactionCCL20 protein, humanChemokine CCL20Receptors, CCR6RNA, MessengerRNA, Small InterferingTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID26536229
PMCPMC4633243
OpenAlexW2270601387

What OpenQuestion holds

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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.