Evidence map›Paper›PMID 26598133›Full record

ArticleScientific reports2015

Transgenic mouse model for imaging of interleukin-1β-related inflammation in vivo.

Takao Iwawaki, Ryoko Akai, Daisuke Oikawa, Takae Toyoshima, Mayuko Yoshino, Mitsumi Suzuki, Naoki Takeda, Tomo-o Ishikawa, Yosky Kataoka, Ken-ichi Yamamura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
0.1field-weighted citation impact, top 44% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Nanoreporter for Real-Time Monitoring of Inflammasome Activity and Targeted Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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  5. Review
  6. Article
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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

10 authors at 2 institutions in 1 country.

Takao IwawakiIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Ryoko AkaiIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Daisuke OikawaIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Takae ToyoshimaIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Mayuko YoshinoIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Mitsumi SuzukiIwawaki laboratory, Education and Research Support Center, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Naoki TakedaDivision of Developmental Genetics, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811, Japan.
Tomo-o IshikawaTransGenic Inc, 7-1-14 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Yosky KataokaCellular Function Imaging Team, Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Ken-ichi YamamuraTransGenic Inc, 7-1-14 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Gunma University · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a biological response associated with symptoms of various diseases, and its study is important in gaining an understanding of the pathological conditions of such diseases and in making strategic plans for promoting healing. It is therefore essential to develop technologies for the detection of inflammatory conditions. Interleukin-1β (IL-1β) is a proinflammatory cytokine produced and secreted mainly by monocytes and macrophages in response to inflammatory stimulation. The activation of IL-1β is regulated through transcriptional induction by the promoter and post-translational processing by the inflammasome. Here we have developed a reporter gene to monitor the activation status of IL-1β by using a dual regulation system and, by using the reporter gene, we have established a mouse model that permits low-invasive visualization of the inflammatory status. Previous reporter systems dependent on the transcription or processing of IL-1β show problems in terms of background noise or signal specificity. Our reporter system overcomes these weaknesses by combining advantages from regulation by a promoter and processing of IL-1β. Our mouse model detected specific physiological inflammation in the liver and pancreas caused by hepatitis or pancreatitis models, respectively. Our reporter gene and mouse model are therefore expected to become useful bioresources for future medical science.

Indexed as

AnimalsDisease Models, AnimalGenes, ReporterHepatitisInflammasomesInterleukin-1betaLipopolysaccharidesLiverLuciferasesMiceMice, Inbred C57BLMice, TransgenicPancreasPancreatitisRAW 264.7 CellsInflammasomesInterleukin-1betaLipopolysaccharidesLuciferases

Identifiers

PMID26598133
PMCPMC4657042
OpenAlexW2411777726

What OpenQuestion holds

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LicenceCC BY
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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.