Evidence map›Paper›PMID 35198577›Full record

ReviewFrontiers in medicine2022

Contribution of the Gut Microbiota to Intestinal Fibrosis in Crohn's Disease.

Daisuke Watanabe, Nobuhiko Kamada

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  12. Immune network · 2024
    Article
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  17. Current and future aspects of IBD research and treatment: The 2022 perspective.Frontiers in gastroenterology (Lausanne, Switzerland) · 2022
    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

2 authors at 2 institutions in 2 countries.

Daisuke WatanabeDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States.
Nobuhiko KamadaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States.
Osaka University · JPUniversity of Michigan–Ann Arbor · US

Funding

The role of IL-1ß-inducing pathobionts in the pathogenesis of Crohn’s diseaseR01DK108901 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Nobuhiko Kamada · 2017 to 2026
$3.8M
Novel biomaterials for IBD treatmentR01DK125087 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO, MOON, JAMES J. · 2020 to 2023
$2.5M
The link between oral bacteria and gut diseaseR01DK119219 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO · 2019 to 2022
$1.6M
Periodontitis and extra-oral mucosal inflammationR21AI142047 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO · 2019 to 2020
$429k
NIAID NIH HHS R21 AI142047NIDDK NIH HHS R01 DK108901NIDDK NIH HHS R01 DK119219NIDDK NIH HHS R01 DK125087
6 · The paper itself

Abstract

In Crohn's disease (CD), intestinal fibrosis is a critical determinant of a patient's prognosis. Although inflammation may be a prerequisite for the initiation of intestinal fibrosis, research shows that the progression or continuation of intestinal fibrosis can occur independently of inflammation. Thus, once initiated, intestinal fibrosis may persist even if medical treatment controls inflammation. Clearly, an understanding of the pathophysiological mechanisms of intestinal fibrosis is required to diminish its occurrence. Accumulating evidence suggests that the gut microbiota contributes to the pathogenesis of intestinal fibrosis. For example, the presence of antibodies against gut microbes can predict which CD patients will have intestinal complications. In addition, microbial ligands can activate intestinal fibroblasts, thereby inducing the production of extracellular matrix. Moreover, in various animal models, bacterial infection can lead to the development of intestinal fibrosis. In this review, we summarize the current knowledge of the link between intestinal fibrosis in CD and the gut microbiota. We highlight basic science and clinical evidence that the gut microbiota can be causative for intestinal fibrosis in CD and provide valuable information about the animal models used to investigate intestinal fibrosis.

Indexed as

adherent-invasive Escherichia coli (AIEC)animal modelCrohn's diseasegut microbiotaintestinal fibrosis

Identifiers

PMID35198577
PMCPMC8859331
OpenAlexW4210407000

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.