Evidence map›Paper›PMID 28474507›Full record

ArticleImmunity, inflammation and disease2017

IL-17F induces IL-6 via TAK1-NFκB pathway in airway smooth muscle cells.

Masayuki Nakajima, Mio Kawaguchi, Kyoko Ota, Junichi Fujita, Satoshi Matsukura, Shau-Ku Huang, Yuko Morishima, Yukio Ishii, Hiroaki Satoh, Tohru Sakamoto and 1 more

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role of Th17 cells in psoriasis.Immunologic research · 2020
    Review
  8. Review
  9. Regulation of IL-17A and implications for TGF-β1 comodulation of airway smooth muscle remodeling in severe asthma.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  10. 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

11 authors at 3 institutions in 3 countries.

Masayuki NakajimaDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Mio KawaguchiDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Kyoko OtaDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Junichi FujitaDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Satoshi MatsukuraRespiratory Disease Center, Showa University Northern Yokohama Hospital, Kanagawa, Japan.
Shau-Ku HuangAsthma and Allergy Center, Johns Hopkins University, Baltimore, Maryland, USA.
Yuko MorishimaDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Yukio IshiiDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Hiroaki SatohDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Tohru SakamotoDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Nobuyuki HizawaDepartment of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
University of Tsukuba · JPNational Health Research Institutes · TWShowa University Northern Yokohama Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionInterleukin (IL)-17F plays a critical role in the pathophysiology of asthma. However, the precise role of IL-17F in airway smooth muscle cells (ASMCs) and its regulatory mechanisms remain to be defined. Therefore, we sought to investigate the expression of IL-6 by IL-17F and the involvement of transforming growth factor β-activated kinase 1 (TAK1) and nuclear factor (NF)-κB by in ASMCs.

methodsASMCs were cultured in the presence or absence of IL-17F. The expression of IL-6 gene and protein was analyzed using real-time PCR and ELISA, and the activation of TAK1 and NF-κB was detected by Western blotting. The effect of TAK1 inhibitor 5Z-7-oxozeaenol and NF-κB inhibitor BAY 11-7082 on the expression of IL-6 was investigated. Finally, the short interfering RNAs (siRNAs) targeting TAK1 and a subunit of NF-κB, p65 were transfected into ASMCs.

resultsThe expression of IL-6 gene and protein was significantly induced by IL-17F. IL-17F activated TAK1 and NF-κB in ASMCs. Transfection of siRNAs targeting TAK1 abolished IL-17F-induced phosphorylation of p65. Both 5Z-7-oxozeaenol and BAY 11-7082 significantly inhibited IL-17F-induced IL-6 production in a dose-dependent manner. Similarly, transfection of the cells with siRNAs targeting TAK1 and p65 inhibited the expression of IL-6.

conclusionsCollectively, these results provided evidence supporting the potential importance of the Th17-ASMCs crosstalk via the IL-17F-IL-6 axis in airway inflammation and as a candidate pharmacological target for airway inflammatory diseases such as asthma.

Indexed as

AsthmaHumansInterleukin-17Interleukin-6LactonesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMAP Kinase Signaling SystemMyocytes, Smooth MuscleNF-kappa BNitrilesResorcinolsSulfonesZearalenone3-(4-methylphenylsulfonyl)-2-propenenitrile7-oxozeanolIL17F protein, humanIL6 protein, humanInterleukin-17Interleukin-6LactonesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BNitrilesResorcinolsSulfonesZearalenoneIL-17FNF-κBTAK1

Identifiers

PMID28474507
PMCPMC5418132
OpenAlexW2594108584

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.