Evidence map›Paper›PMID 25492478›Full record

ArticleMucosal immunology2015

Intestinal neuroendocrine cells and goblet cells are mediators of IL-17A-amplified epithelial IL-17C production in human inflammatory bowel disease.

M Friedrich, J Diegelmann, J Schauber, C J Auernhammer, S Brand

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

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  20. Intestinal Enteroendocrine Cells: Present and Future Druggable Targets.International journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

M Friedrich1] Department of Medicine II-Grosshadern, Ludwig-Maximilians-University (LMU) Munich, Munich, Germany [2] Clinic for Preventive Dentistry and Parodontology, LMU Munich, Munich, Germany.
J Diegelmann1] Department of Medicine II-Grosshadern, Ludwig-Maximilians-University (LMU) Munich, Munich, Germany [2] Clinic for Preventive Dentistry and Parodontology, LMU Munich, Munich, Germany.
J SchauberDepartment of Dermatology and Allergy, LMU Munich, Munich, Germany.
C J AuernhammerDepartment of Medicine II-Grosshadern, Ludwig-Maximilians-University (LMU) Munich, Munich, Germany.
S BrandDepartment of Medicine II-Grosshadern, Ludwig-Maximilians-University (LMU) Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-17C is a novel member of the IL-17 cytokine family. Its function in human inflammatory bowel disease (IBD) remains elusive as its role in colonic inflammation is entirely derived from murine models. We aimed to analyze the role of IL-17C in human IBD, focusing on T helper type 17 (Th17) cell- and intestinal epithelial cell (IEC)-dependent mechanisms. IL-17C mRNA (P=0.005), serum levels (P=0.008), and colonic staining intensity (P=0.004) is increased in active IBD. Serum IL-17C levels are modified by IL23R genotypes and IL-17C mRNA correlates (r>0.5, P<0.001) with IL-17A, tumor necrosis factor (TNF)-α, C-C motif chemokine ligand 20 (CCL20) and IL-23 mRNA in the inflamed colon of IBD patients. In the inflamed colon, IL-17C is produced by enteroendocrine and goblet cells, with contrary polar cytosolic localization of IL-17C within the cellular axis. In these two cell types, IL-17A strongly amplifies TNF-α-induced IL-17C production. On the molecular level, IL-17C production in IECs is dependent on TNF-α-activated nuclear factor-κB, extracellular signal-regulated kinase-1/2 and p38, and IL-17A-activated Akt, monocyte chemotactic protein-induced protein 1, and C/EBPδ. IL-17C upregulates the Th17 chemoattractant CCL20 in IECs. In summary, our findings support the involvement of IL-17A-amplified IL-17C production by enteroendocrine and goblet cells in the pathogenesis of active IBD, revealing an interaction between the neuroendocrine system and the Th17 pathway in human IBD.

Indexed as

Autocrine CommunicationBiomarkersCCAAT-Enhancer-Binding ProteinsChromogranin AConnexin 43CytokinesEpithelial CellsGene ExpressionGenotypeGoblet CellsHumansInflammatory Bowel DiseasesInterleukin-17Mitogen-Activated Protein KinasesNeuroendocrine CellsNF-kappa BACT1 proteinBiomarkersCCAAT-Enhancer-Binding ProteinsChromogranin AConnexin 43CytokinesIL23R protein, humanInterleukin-17Mitogen-Activated Protein KinasesNF-kappa BPeptide FragmentsProto-Oncogene Proteins c-aktReceptors, InterleukinRibonucleasesRNA, MessengerTranscription FactorsTumor Necrosis Factor-alphaZC3H12A protein, human

Identifiers

PMID25492478
OpenAlexW1990342706

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.