Evidence map›Paper›PMID 32793240›Full record

ReviewFrontiers in immunology2020

Our Evolving Understanding of Kawasaki Disease Pathogenesis: Role of the Gut Microbiota.

Kazunari Kaneko, Shohei Akagawa, Yuko Akagawa, Takahisa Kimata, Shoji Tsuji

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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  17. Gut Microbiota Alterations in Patients With Kawasaki Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025
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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 1 institution in 1 country.

Kazunari KanekoDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.
Shohei AkagawaDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.
Yuko AkagawaDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.
Takahisa KimataDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.
Shoji TsujiDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kawasaki disease (KD) was first described by Dr. Tomisaku Kawasaki in 1967. The etiology of KD has been studied comprehensively but remains largely unknown. The disease seems to result from the interplay of genetic and environmental susceptibility factors with infectious triggers, followed by a subsequent abnormal immune response characterized by increased levels of inflammatory cytokines and chemokines during the acute phase. Evidence has mounted to suggest that an imbalance between T helper 17 cells (Th17s) and regulatory T cells (Tregs) is associated with aberrant immune responses in KD. Recent advances in culture-independent techniques for detection and identification of intestinal commensal bacteria enabled the discovery that Th17 and Treg differentiation are regulated by short chain fatty acids (SCFAs), in particular butyrate, produced by the gut microbiota. This finding provided a mechanistic link between dysbiosis, defined as changes in the composition of the gut microbiota, and various inflammatory diseases. On this basis, we propose that dysbiosis, with reduced production of SCFAs leading to imbalances of Th17s/Tregs, could be involved in the etiology of KD. A pilot study supported this hypothesis, as only fecal concentrations of butyrate were significantly reduced in KD patients among SCFAs. This evolving perspective prompted us to undertake metagenomic analyses of bacterial DNA from the feces of KD patients who were antibiotic-naïve at diagnosis. Simultaneous measurements of Th17s/Tregs in peripheral blood and SCFA concentrations in feces would provide valuable information regarding the association between dysbiosis and dysregulated immune responses in KD.

Indexed as

Disease SusceptibilityGastrointestinal MicrobiomeAnimalsDysbiosisEnvironmentGenetic Predisposition to DiseaseHumansMucocutaneous Lymph Node SyndromeRisk FactorsT-Lymphocyte Subsetsallergydysbiosisgut microbiotaKawasaki diseaseregulatory T cellT helper 17 cell

Identifiers

PMID32793240
PMCPMC7393004
OpenAlexW3043939625

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.