Evidence map›Paper›PMID 22994872›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2012

Toll-like receptor 5 engagement induces interleukin-17C expression in intestinal epithelial cells.

Eunok Im, Jane Jung, Sang Hoon Rhee

Abstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Flagellar regulation in enterotoxigenicInfection and immunity · 2026
    Article
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  5. Transcriptome Sequencing RevealsCurrent issues in molecular biology · 2023
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  20. IL-17C expression in nasal epithelial cells of chronic rhinosinusitis with nasal polyposis.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2014
    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

3 authors at 2 institutions in 2 countries.

Eunok ImSchool of Pharmacy, Pusan National University, Busan, Korea.
Jane Jung
Sang Hoon Rhee
University of California, Los Angeles · USPusan National University · KR

Funding

Innate Immune Response and Intestinal InflammationK01DK079015 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RHEE, SANG HOON · 2008 to 2010
$450k
NIDDK NIH HHS DK079015
6 · The paper itself

Abstract

The family of interleukin-17 (IL-17) cytokine is the essential inflammatory mediator that influences the pathophysiology of various inflammatory diseases. Many studies focused on investigating the expression, signaling, and biological impacts of IL-17A and IL-17F, and the neutralization of these cytokines exhibited some promising results in clinical trials. In contrast, the expression resources and physiological relevance of IL-17C remained to be studied. In this study, through a microarray approach conducted with nontransformed human colonic epithelial cells (NCM460), we found that bacterial flagellin stimulation elicited potent IL-17C mRNA expression. We also confirmed that IL-17C protein production was strongly induced by flagellin in these cells. Flagellin-induced IL-17C expression was also observed in human colon adenocarcinoma cells such as DLD-1 and HT-29, indicating that IL-17C could be a signature inflammatory cytokine from intestinal epithelial cells in response to flagellin. Since inhibited in TLR5-, or MyD88- or TRIF-silenced cells, flagellin-induced IL-17C expression was specifically mediated by TLR5 and, subsequently, MyD88 and TRIF adaptor molecules. Furthermore, in line with inflammatory nature of IL-17, we found that IL-17C expression was substantially enhanced in the intestinal tissues from Ulcerative colitis patients. Given the facts that TLR5 is a key pattern recognition receptor which mediates microbial recognition in the intestinal epithelium and IL-17C turned out to be a unique member of the IL-17 family expressed in intestinal epithelial cells on TLR5 activation, our study may provide an important clue on understanding how intestinal microbes would contribute to an inflammatory program in the gut.

Indexed as

Up-RegulationAdaptor Proteins, Vesicular TransportAdenocarcinomaCell LineCell Line, TumorColitis, UlcerativeColonic NeoplasmsCrohn DiseaseFemaleFlagellinGene SilencingHumansInterleukin-17Intestinal MucosaMaleMyeloid Differentiation Factor 88Adaptor Proteins, Vesicular TransportFlagellinIL17C protein, humanInterleukin-17MYD88 protein, humanMyeloid Differentiation Factor 88Neoplasm ProteinsRNA, MessengerRNA, Small InterferingTICAM1 protein, humanTLR5 protein, humanToll-Like Receptor 5

Identifiers

PMID22994872
PMCPMC3514012
OpenAlexW2093434060

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.