Evidence map›Paper›PMID 33833754›Full record

ReviewFrontiers in immunology2021

Intestinal Dysbiosis and Autoimmune Pancreatitis.

Tomoe Yoshikawa, Tomohiro Watanabe, Ken Kamata, Akane Hara, Kosuke Minaga, Masatoshi Kudo

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05722678 (Study and Analysis on the Characteristics of Intestinal Microorganisms and Serum Metabolites in Patients With Acute Pancreatitis Complicated With COVID-19), which is not on this map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.6field-weighted citation impact, top 7% 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.

NCT05722678 unknown statusnot on this mapstarted 2023, after this paper: background citation

Study and Analysis on the Characteristics of Intestinal Microorganisms and Serum Metabolites in Patients With Acute Pancreatitis Complicated With COVID-19

TypeobservationalSponsorYuansong SunRan2023 to 2023Enrolled30ConditionsAcute Pancreatitis, 2019 Novel Coronavirus Infection
3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Insights into Microbiota in Sjögren's Syndrome.Medicina (Kaunas, Lithuania) · 2023
    Review
  7. Review
  8. The oral microbiome in autoimmune diseases: friend or foe?Journal of translational medicine · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Review
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

6 authors at 1 institution in 1 country.

Tomoe YoshikawaDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Tomohiro WatanabeDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Ken KamataDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Akane HaraDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Kosuke MinagaDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Masatoshi KudoDepartment of Gastroenterology and Hepatology, Kindai University, Faculty of Medicine, Ohno-Higashi, Osaka-Sayama, Japan.
Kindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune pancreatitis (AIP) is a chronic fibro-inflammatory disorder of the pancreas. Recent clinicopathological analysis revealed that most cases of AIP are pancreatic manifestations of systemic IgG4-related disease (IgG4-RD), a newly established disease characterized by enhanced IgG4 antibody responses and the involvement of multiple organs. Although the immuno-pathogenesis of AIP and IgG4-RD has been poorly defined, we recently showed that activation of plasmacytoid dendritic cells (pDCs) with the ability to produce large amounts of IFN-α and IL-33 mediates chronic fibro-inflammatory responses in experimental and human AIP. Moreover, M2 macrophages producing a large amount of IL-33 play pathogenic roles in the development of human IgG4-RD. Interestingly, recent studies including ours provide evidence that compositional alterations of gut microbiota are associated with the development of human AIP and IgG4-RD. In addition, intestinal dysbiosis plays pathological roles in the development of chronic pancreatic inflammation as dysbiosis mediates the activation of pDCs producing IFN-α and IL-33, thereby causing experimental AIP. In this Mini Review, we focus on compositional alterations of gut microbiota in AIP and IgG4-RD to clarify the mechanisms by which intestinal dysbiosis contributes to the development of these disorders.

Indexed as

AnimalsAutoimmune PancreatitisDendritic CellsDysbiosisGastrointestinal MicrobiomeHumansImmunoglobulin G4-Related DiseaseInterferon-alphaInterleukin-33Models, AnimalInterferon-alphaInterleukin-33autoimmune pancreatitisdysbiosisIgG4-related diseaseintestinal microbiotaplasmacytoid dendritic cells

Identifiers

PMID33833754
PMCPMC8021793
OpenAlexW3139273046

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.